Selected Topics in

Pediatrics
for Practitioners
Selected Topics in
Pediatrics
for Practitioners
Editor-in-Chief
A Parthasarathy
Rtd. Senior Clinical Professor of Pediatrics and
Deputy Superintendent
Madras Medical College and Institute of
Child Health and Hospital for Children
Egmore, Chennai
Academic Editors
P Ramachandran
Asst Prof of Pediatrics
Madras Medical College and Institute of
Child Health and Hospital for Children
Egmore, Chennai
S Thangavelu
Asst Prof of Pediatrics
Madras Medical College and Institute of
Child Health and Hospital for Children
Egmore, Chennai

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Selected Topics in Pediatrics for Practitioners

© 2004 A Parthasarathy, P Ramachandran, S Thangavelu
All rights reserved. No part of this publication should be reproduced, stored in a retrieval
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This book has been published in good faith that the material provided by the
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First Edition : 2004

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 Contributors

RK Agarwal MKC Nair

Director, RK Hospital Director, Child Development Center,
Udaipur SAT Medical College Campus
Ananthalakshmi Thiruvananthpuram
Hony Director, Indian Council for
Child Welfare TN, Chennai A Parthasarathy
Rtd. Senior Clinical Professor of
RK Bagdi Pediatrics and
Professor of Pediatric Surgery Deputy Superintendent
Madras Medical College and Madras Medical College and Institute of
Institute of Child Health and Hospital for Child Health and Hospital for Children
Children Egmore, Chennai Egmore, Chennai
Swati Y Bhave
Senior Consultant Pediatrician P Ramachandran
Apollo Indraprastha Hospitals Assistant Prof of Pediatrics
New Delhi Madras Medical College and Institute of
N Deivanayagam Child Health, Chennai
Rtd Professor of Pediatrics and HOD P Ramadevi
Clinical Epidemiology Unit Professor of Pediatrics
Director and Superintendent (Incharge) Director and Superintendent
Madras Medical College and Institute of Madras Medical College and Institute of
Child Health and Hospital for Children Child Health and Hospital for Children
Egmore, Chennai Egmore, Chennai
Piyush Gupta
Professor of Pediatrics, University College P Sabapathy Raj
of Medicine, New Delhi Asst Prof of Pediatrics
MP Jeyapaul Madras Medical College and Institute of
Rtd Prof of Pediatrics and Director and Child Health and Hospital for Children
Superintendent Egmore, Chennai
Madras Medical College and Institute of
Child Health and Hospital for Children HPS Sachdev
Egmore, Chennai Professor of Pediatrics
Maulana Azad Medical College
G Kumaresan New Delhi
Prof of Child Neurology
Madras Medical College and Institute of VS Sankaranarayanan
Child Health and Hospital for Children Rtd Prof and HOD of Pediatric
Egmore, Chennai Gastroenterology
Madras Medical College and Institute of
Roopa Nagarajan
Child Health and Hospital for Children
HOD Department of Speech, Language
Egmore, Chennai
and Hearing Sciences,
Sri Ramachandra Medical College and Ramesh Santhanakrishnan
Research Institute Medical Director, BRS Hospitals
(Deemed University), Porur, Chennai Chennai
vi Selected Topics in Pediatrics for Practitioners

S Srinivas Chandra Thanikachalam

Consultant, BRS Hospitals Hony Joint Secretary
Chennai Indian Council for Child Welfare (TN)
Shenoy Nagar, Chennai
TU Sukumaran
Professor of Pediatrics, Superintendent BR Thapa
Institute of Maternal Child Health Addl Prof of Pediatric Gastroenterology
Kottayam Medical College Postgraduate Institute of Medical
Kottayam Education and Research
Chandigarh
PG Sundararaman
Lecturer in Endocrinology P Venkataraman
Madras Medical College and Asst Professor of Pediatrics
Institute of Obstetrics and Gynecology Madras Medical College and Institute of
Chennai Child Health and Hospital for Children
Egmore, Chennai
S Thangavelu
Asst Prof of Pediatrics M Vijayakumar
Madras Medical College and Institute of Consultant Nephrologist
Child Health and Hospital for Children, Kanchi Kamakoti
Egmore, Chennai CHILDS Trust Hospital, Chennai
 Foreword

The Practitioners of child health need updating of their knowledge on

current concepts in the management of common childhood illnesses in
day-to-day practice. I am sure this book entitled Selected Topics in Pediatrics
for Practitioners, will fulfil this need.
The contributors have taken great pains to give updated information
in a reader for friendly manner. A busy practitioner today needs only a
desktop reference booklet rather than an exhaustive and detailed textbook.
With this in mind, topics have been carefully chosen and named “Selected
Topics” so that the practitioner’s time will be saved to make quick reference.
I congratulate the editors for having done an excellent job in choosing
the right topics and having them written by the experts in the related
field. I am confident that this book will satisfy the expectations of the
reader. I am sure, suitable revision, addition of few more selected topics
and needful updating will enhance the value of this book in its future
editions.
Dr MKC Nair
President (2004)
Indian Academy of Pediatrics
 Preface

Today Pediatrics in India is being practiced by family physicians and

qualified pediatricians. Upcountry pediatricians as well as a family
physicians, need a ready reckoner, which they can quickly refer before
decision making in the management of their child patient. An attempt
has, therefore, been made in this book to include selected topics, which
are of day-to-day importance for pediatric practitioners and present them
in a concise manner with updated information.
A wide range of 28 topics starting from ‘Principles and Practices of
Pediatrics’ to ‘Pediatrician in the Year 2033’ have been chosen apart from
systemic infections ‘Essential Newborn Care’, ‘Practical Aspects of Growth
and Development’, ‘Infant and Young Child Feeding’ and ‘Immunization
Practices’ which need constant updating because of changing concepts;
have been included. The topics on ‘Childhood Communication Disorders’,
‘Child Adoption in India’, ‘Pediatrician and Adoption’ are aimed at imparting
new knowledge to the practitioner. To impress upon the practicing
pediatrician that effective medical research can also be a part of office
practice ‘Medical Research in Office Practice’ has also been included. The
topic ‘Pediatric Surgical Referrals’ will act as a ready reckoner. The 6
annexures added to the main text should also be a ready source of
information to the busy practitioner.
It is our fervent hope that this newborn will serve the needs of family
physicians and pediatricians in their day-to-day practice. Your valuable
suggestions are most welcome to improve the quality of the book in future
reprints/editions.
A Parthasarathy
P Ramachandran
S Thangavelu
 Acknowledgements

The editors would like to place on record their appreciation and gratitude
to the following who helped in the completion of this project.
1. Prof N Deivanayagam, Prof VS Sankaranarayanan, Prof MP Jeyapaul,
Prof G Kumaresan, Prof RK Bagdi Dr Sabapathy Raj, Prof Roopa
Nagarajan, Dr Mrs Ananthalakshmi, Mrs Chandra Thanikachalam,
Chennai, Prof TU Sukumaran, Kottayam, Prof BR Thapa, Chandigarh,
our Guest contributors.
2. Prof HPS Sachdev, Professor of Pediatrics, Maulana Azad Medical
College and Prof Piyush Gupta, Professor Pediatrics, University College
of Medicine, New Delhi and Dr Ramesh Santhanakrishnan, Medical
Director, BRS Hospitals, Chennai and M/s Jaypee Brothers Medical
Publishers (P) Ltd, New Delhi for permitting to reproduce the tables
from IAP Textbook of Pediatrics 2003 edition.
3. Prof Suraj Gupte, Prof Arun Gupta, Prof Shameem Ahamed whose
tables have been adapted and reproduced.
4. Mr Kiran, Mrs Anuradha and Miss Meenakshi of Anu Vision Media,
Chennai and Mr Venkat and Mrs Padmaja Venkat of Shabari computers,
Chennai for executing the manuscript formatting at short notice.
5. Mr N Suresh, Mr G Suresh, Miss M Meenakshi, Miss D Lakshmi,
Miss V Seshamma, Miss D Rajeswari, Mr Rajkumar and Mr S Paulraj
for help rendered in typesetting and formatting the manuscript and
for co-ordination.
6. Mrs Nirmala Parthasarathy and Kavitha Balaji for secretarial assistance.
7. Mr PV Chandrasekar, Mr KA Shankaranarayan, Mr A Sri Ramulu for
their dedicated services and co-ordination.
8. Mr JP Vij, Chairman and Managing Director and Mr Tarun Duneja,
General Manager (Publishing) of Jaypee Brothers Medical Publishers
(P) Ltd, New Delhi for designing, developing, typesetting, printing
and publishing the book at record time.
9. Mr Anil Pillai (Branch Manager), Mr A Senthil Kumar (Assistant Branch
Manager), Mr M Anbukkarasan (Sales Executive), Mr R Jayanandhan
(Author Co-ordinator), Miss N Ramya, Miss AV Gayathri Krishna, Mr
S Rajesh, Mrs K Vasanthi of Jaypee Brothers Medical Publishers,
Chennai Branch Office for help rendered and co-ordination.
 Contents

1. Principles and Practice of Pediatrics in India 1

A Parthasarathy
2. Essential Newborn Care 4
P Ramadevi, P Ramachandran
3. Practical Aspects of Growth and Development
in Early Childhood 29
S Thangavelu
4. Infant and Young Child Feeding 42
A Parthasarathy
5. Immunization in Practice 49
A Parthasarathy
6. Approach to the Diagnosis and Management
of a Febrile Child 62
S Thangavelu
7. Newer Concepts in Epilepsy Management 74
G Kumaresan
8. Recent Trends in the Diagnosis and Management
of Bacterial Meningitis 79
G Kumaresan
9. Changing Trends in Prophylaxis of Rheumatic Fever 82
P Sabapathy Raj
10. Recent Concepts in the Management of Congestive
Cardiac Failure 88
P Sabapathy Raj
11. Current Trends in Diagnosis and
Management of Bronchial Asthma 94
TU Sukumaran
12. Childhood Tuberculosis— Management Guidelines 114
MP Jeyapaul, A Parthasarathy
13. Management of Acute Diarrhea 123
VS Sankaranarayanan, S Srinivas
14. Neonatal Cholestasis Syndrome Practical Approach 132
BR Thapa
15. Constipation and Encopresis in Infants and Children 147
BR Thapa
16. Urinary Tract Infection in Children 160
M Vijayakumar
17. Acute Nephritis and Nephrotic Syndrome 167
P Ramachandran
xiv Selected Topics in Pediatrics for Practitioners

18. Management of Common Endocrine

Problems— Current Concepts 173
P Venkataraman, PG Sundararaman
19. Recognition and Initial Management of Critically Ill Child 189
P Ramachandran
20. Poisoning in Children 196
S Thangavelu
21. Rational Drug Therapy in Pediatric Practice 216
A Parthasarathy
22. Pediatric Surgical Referrals 226
RK Bagdi
23. Designing Medical Research in Office Practice 231
N Deivanayagam
24. Childhood Communication Disorders 237
Roopa Nagarajan
25. Child Adoption in India 263
Chandra Thanikachalam
26. Pediatricians and Adoption 273
Ananthalakshmi
27. Adolescent Care: The Practitioner’s Role 276
MKC Nair, Swati Y Bhave
28. Pediatrician in the Year 2033 321
RK Agarwal

ANNEXURES
Annexure 1 – Normal Laboratory Values 325
HPS Sachdev, Piyush Gupta
Annexure 2 – Fluid Therapy 340
Ramesh Santhanakrishnan
Annexure 3 – Drugs and Drug Dosage 344
Ramesh Santhanakrishnan
Annexure 4 – Vital Statistics—India 355
HPS Sachdev, Piyush Gupta
Annexure 5 – National Socio-demographic Goals for 2010 357

Annexure 6 – Children’s Forum Message—A World Fit for Us 358

Index 361
 1
Principles and Practice of
Pediatrics in India
A Parthasarathy

Pediatrics has been defined as the Art (derived from the beliefs,
judgements, and intutions we could not explain) and Science (derived
from the knowledge, logic and prior experience we could explain) of
treating Childhood Illnesses. In as much as stress has been laid on
Preventive Pediatrics, emergence of pediatrics subspecialties have equally
revolutionized the management of even rare conditions in pediatric
practice. So, a pediatrician of today, has a dual role to play viz.,
community counseling and management of childhood illnesses at the
clinic and health care facility. Ethics for pediatric practice should evolve
around not only ethical practice but also about self discipline, self
determination and above all self confidence. Updating and upgrading
knowledge through continuing medical education in conferences,
seminars, symposia, etc. have since become a compelling necessity.
Whether in office or hospital practice a pediatrician has to be familiar
with all aspects of growth, development, newborn care, immunization,
management of common illnesses including the recent advances and
also equip himself with the knowledge of rare conditions, syndromes,
etc. Communication disorders have first to be recognized by him for
appropriate referrals and remedial follow-up action. The standard
protocols for management of common childhood illnesses laid down by
the World Health Organization from time to time have to be familiarized
by each and every practicing pediatrician.
Rational use of drugs and more so of anti-microbials have become
the order of the day. Caution should be exercised to avoid banned
drugs. Adverse events following drug/vaccine administration should
be brought to the notice of the Regional Health Authority concerned
and appropriate follow-up action taken. Professional bodies like the
American Academy of Pediatrics, British Pediatric Association, Canadian
Pediatric Society, Indian Academy of Pediatrics to name a few, have
come out with consensus statements for management of common
childhood illnesses and ample guidelines have been outlined. Equally
important is to avoid prescribing irrational fixed drug combinations.
2 Selected Topics in Pediatrics for Practitioners

As observed earlier, pediatricians of today whether in Government

service or in Private practice have to play a dual role of “One foot in
the hospital and the other in the community”. There are several National
Child Health Programs, which need active coordination and cooperation
of pediatricians. To mention a few the post independence Maternal and
Child Health (MCH) Program, the Expanded Program on Immunization
(EPI), the Universal Immunization (UIP) Program, the Acute Respiratory
Infections Control (ARI) Program, the Acute Flaccid Paralysis (AFP)
Surveillance Program, the Diarrhea Disease Control (DDC) program, the
Child Survival and Safe Motherhood (CSSM) Program, the Reproductive
and Child Health (RCH) Program and the WHO strategy of Integrated
Management of Neonatal and Childhood Illnesses(IMNCI), etc. needed
the practicing pediatricians active support for their implementation.
Their successful implementation with active participation and
cooperation have recorded phenomenal success in reducing neonatal
mortality, infant mortality, under 5 mortality and improved the nutritional
and immunization status of under 5 children. Newer concepts in oral
rehydration therapy (ORT) have significantly reduced morbidity and
mortality following dehydration due to Acute Watery Diarrhea (AWD).
Short course IV fluid therapy has equally revolutionized the concept of
intravenous fluid therapy in diarrheal illness.
Another area, which needs the attention of a practicing pediatrician
today, is the Consumer Protection Act (COPRA) and related issues.
Gross negligence by a practitioner is now punishable under law and
basic minimum facilities for cardiopulmonary resuscitation (CPR) are
mandatory even in office practice. Professional bodies have come out
with insurance schemes for their members. Nevertheless gross omissions
and commissions are being viewed seriously. One has to be familiar
with the sections of COPRA and avoid unnecessary ‘Commissions and
Omissions’.
The medical profession in general today, is under heavy criticism by
public for ‘converting?’ a noble profession into a ‘profit making business
so to say, because of some commissions by few doctors?; the entire
profession has become under strict ‘Public Surveillance’. Gone are the
days when doctors were considered as Demi-Gods or equated with
Gods. Today a pediatrician has to satisfy the parents of his child patient
who pose a volley of questions (both wanted and unwanted or legitimate
and illegitimate) patiently despite the constraints of his pressure on
work and other commitments. So much so, health education becomes
an integral part of the management of any illness especially so if it is
a preventable illness. Whether in hospital or office practice the
pediatrician has a moral responsibility to explain to the parent about the
 Principles and Practice of Pediatrics in India 3

cause of diseases, its probable course, prognosis, management and follow

up advice with appropriate preventive and nutrition counseling.
Let us, therefore, redefine our responsibilities as a responsible
pediatrician: dedicate ourselves to the Hippocrates oath we have pledged
at the time of our graduation; discharge our duties with compassion and
competence; dissociate ourselves from any activity that may invite
criticism or comments and thus contribute our mite to the welfare of
future citizens of our great country, whose care and nurture are in our
hands.

BIBLIOGRAPHY
1. Carol Bellamy: The state of the World’s Children 2003: The Executive Director’s
Office: United Nation’s Children’s Fund, UNICEF House, 3 UN Plaza, New
York, NY 10017, USA.
2. Report on the meeting of under 18 delegates to the UN special session on
children. New York, 5-7 May 2002 – UNICEF Publication, October 2002.
 2
Essential Newborn Care
P Ramadevi, P Ramachandran

Optimal newborn care is of great importance as deaths in newborn

period contribute to nearly two thirds of infant mortality in our country.
Knowledge and skills on basic newborn care are essential for all health
care providers. Newborn care cannot be improved without improving
maternal health and nutrition. Maternal health is derived from good
health of adolescent girl, which in turn depends on healthy newborn
girl.

Fig. 2.1
Definitions and Nomenclature
1. Birth weight groups
Low birth weight (LBW) : < 2500 grams
Very low birth weight (VLBW) : < 1500 grams
Extremely low birth weight (ELBW) : < 1000 grams
2. Gestational age groups
Preterm : Gestational age < 37 weeks
Term : 37 weeks – 41 weeks
Postterm : 42 weeks or more
3. Birth weight and gestational age
Small for gestational age (SGA) : < 10th percentile
babies Weight for gestational age
4. Appropriate for gestational age (AGA) : 10-90th percentile
Large for gestational age (LGA) : > 90th percentile
5. Perinatal period From 28th week of gestation upto 7th day after birth
6. Neonatal period Birth—28 days
 Essential Newborn Care 5

7. Early neonatal period First 7 days of life

8. Perinatal mortality rate (PMR)
Total deaths in perinatal period weighing > 1000 gm
_______________________________________________
× 1000 gm
Total number of births weighing > 1000 gm
9. Neonatal mortality rate (NMR)
Death of babies > 1000 gm in 28 days of life
_________________________________________
× 1000 gm
Total live births weighing > 1000 gm

Leading causes of neonatal mortality in India

a. Bacterial infection (sepsis, pneumonia)
b. Low birth weight
c. Birth asphyxia
d. Congenital malformations

Care of Normal Newborn in Labour Room

Principles of Neonatal Care at Birth
• Establishment of effective respiration
• Prevention of hypothermia
• Initiation of breastfeeding
• Prevention of infection
• Identification of high risk neonates
The newborn is given a warm welcome both physically and
emotionally.

Requirements for Normal Delivery

— 2 prewarmed clean towels
— Suction devices (bulb sucker, de Lee suction trap)
— Clean gauze pieces, cotton balls
— Sterile scissors
— Cord clamp
— Kidney tray
— Catheters (8F NG tubes) to check oesophageal and anal patency.

Stepwise Approach of Immediate Newborn Care

1. The newborn baby is received on a prewarmed towel, dried
thoroughly including the scalp and covered with another warm clean
towel exposing only the face (2 towel method). During drying vernix
covering the baby need not be removed as it forms a protective coat.
2. Position the baby and gentle suctioning of mouth, orpharynx and
then nose is done with a bulb sucker or catheter.
3. Evaluate respiration, heart rate and colour of the baby Most babies
cry well, are pink and active.
6 Selected Topics in Pediatrics for Practitioners

4. Umbilical cord is cut with sterile scissors and cord clamp/tie is

applied.
Cleans (5 C’s) are essential for any delivery—clean surface, clean hands,
clean blade, clean tie and clean cord
5. Check oesophageal and anal patency.
6. A head to foot examination is done next to find out any major
congenital anomaly
7. If the baby is well, it is kept warm near the mother. Skin to skin and
eye-to-eye contact with mother is encouraged and the baby is allowed
to suckle at breast immediately after birth when he/she is quite
active. This also helps the newborn to feel secure and warm.
8. Weight the baby and record weight. Put an identity tag.

Ten Points to Prevent Heat Loss at Birth

• Warming the delivery room (28°C)
• Pre heated micro environment
• Avoid drought of air (fans, air conditioners, etc.)
• Cover legs/body in breech delivery while waiting for head to deliver
• Dry the infant thoroughly
• Remove wet linen
• Proper wrapping including head
• Swaddle the baby while carrying baby from one place to another
even within delivery room or for displaying the baby to parents
• Keep with mother
• Early breastfeeding.

Examination of Newborn after Normal Delivery

A detailed examination of newborn is conducted at birth, 24 hours later
and at the time of discharge. The examination is aimed towards assessing
the well being of baby and identifying life threatening congenital
malformations and birth injuries.

Fig. 2.2: Baby well swaddled

 Essential Newborn Care 7

At birth
Head to food localization should be done to identify congenital anomalies.
At 24 hours
1. Vital signs Normal respiratory rate is 40-60/minute and is thoraco-
abdominal. Breathing is usually periodic and irregular. Heart rate
varies from 120-160/minute. Trunk and extremities usually feel warm
when palpated with back of the hand. Extremities should look pink.
2. Colour, activity and alertness While awake, the baby should be active
and moving the limbs well. Appearance of jaundice within 24 hours
denotes a serious problem.
3. Gestational assessment This is done based on physical and neurologic
characteristics.
4. Skull look for caput succedaneum and cephalhematoma.
a. Caput succedaneum Boggy, diffuse scalp swelling over presenting
part seen at birth. Disappears spontaneously over next few days.
b. Cephalhematoma Subperiosteal collection of blood during delivery.
Fluctuant swelling, does not cross midline and resolves after few
days or weeks. Noninterference needed.
5. Extremities Look for deformities and normal movement of limbs.
6. Abdomen and genitalia Masses are looked for. Look at genitals for
undescended testes and hydrocele. Prepuce is nonretractable in normal
babies.
At discharge
1. Reexamine for congenital anomalies and birth injuries.
2. Confirm that the child’s colour and respiration are normal.
3. Identify any feeding difficulty. Teach the mother about positioning
of the baby and proper attachment at breast.

Resuscitation of Asphyxiated Newborn at Birth

Most of the newborns adapt for extrauterine life very quickly after birth.
Establishment of effective spontaneous breathing is crucial for survival
of newborn. About 3.5 to 7.5 percent of newborns may require some
assistance in establishing respiration at birth. Asphyxia refers to a
combination of hypoxia, hypercarbia and metabolic acidosis. For clinical
purpose, birth asphyxia should be diagnosed when ‘baby has gasping
or no breathing at 1 minute after birth’. This corresponds to a 1 minute
apgar score of 3 or less. The presence of certain risk factors should alert
the doctor to anticipate birth asphyxia and make proper preparations
for resuscitation. Rarely problems may arise even when these are no risk
factors. Hence each delivery should be attended by a doctor/health care
provider who can resuscitate a newborn.
8 Selected Topics in Pediatrics for Practitioners

Certain risk factors for birth asphyxia are:

Antepartum Factors
1. Placental insufficiency: Toxemia, hypertension, diabetes mellitus, post
maturity
2. Bad obstetric history: Previous abortions, still births or neonatal death
3. Malpresentation and abnormal lie
4. Poor fetal growth
5. Multiple gestation
6. Antepartum hemorrhage
7. Poly/oligo hydramnios
8. Maternal disease
Intrapartum Factors
1. Preterm labor
2. Cord prolapse
3. Meconium stained liquor
4. Prolonged labor (more than 24 hours)
5. Prolonged rupture of membranes (more than 12 hours)
6. Evidence of fetal distress
Apgar Scoring
The APGAR score is a method to assess newborn’s condition at birth.
Apgar scoring is conventionally done at 1 minute, 5 minutes and for
longer if necessary. However, resuscitation should not be delayed till the
1 minute assessment in a depressed baby. Apgar score is not used to
determine the need for resuscitation and the type of resuscitation steps.
Apgar score is more useful for prognosticating neurodevelopmental
outcome.
Evaluation of newborn is based on
• Respiration
• Heart rate
• Colour
The other two components of Apgar score such as muscle tone and
reflux response are dependent on gestational maturity, cardiorespiratory
status and neurologic status.
Apgar Score

Sign 0 1 2

Heart rate Absent Slow (<100/mt) > 100/mt

Respirations Absent slow, irregular Good, crying
Muscle tone Limp Partial flexion Well flexed

Contd...
 Essential Newborn Care 9

Contd...

Sign 0 1 2

Reflex irritability None Grimace Cough, sneeze

(to nasal catheter)

Colour Blue/pale Pink centrally, blue peripheries Completely pink

Score > 8 Normal

6-7 mild asphyxia
4-5 moderate asphyxia
< 3 severe asphyxia

Preparation for Resuscitation

For neonatal resuscitation 2 or 3 skilled personnel and equipments should
be available. Protocol for resuscitation, monitoring and transport
arrangements should be prepared in advance. If the place of delivery
does not have adequate facilities for resuscitation of an anticipated high-
risk delivery, it is better to refer the pregnant mother with fetus in utero
to a higher center.

Resuscitation Equipments Needed

1. Suction equipment: Bulb syringe, de Lee suction trap, suction
catheters, 6 F, 8F and 10F, meconium aspirator.
2. Self filling resuscitation bag of 450-500 ml volume with pop-off
valve, proper sized masks for preterm and term newborn
3. Oxygen source with flow meter and tubing
4. Laryngoscope with straight blades No.0 (for preterm) and No.1
(for term); extra bulbs and batteries
5. Endotracheal tubes 2.5, 3.0 and 3.5 size
6. Adhesive solution (Tincture benizoin) and adhesive tape
7. Sterile gloves, sterile scissors
8. Umbilical vein catheter (3.5 or 5 size)
9. Syringe (2 ml, 5 ml, 10 ml), IV cannulas 24 size
10. Radiant warmer or other heat source
11. Drugs: Adrenaline (Epinephrine) 1:10000, normal saline, 10 percent
dextrose and 4.2 percent sodabicarb.

Principles in Resuscitation
ABC’s of resuscitation
• Airway (position and clear)
• Breathing (stimulate to initiate breath)
• Circulation (Heart rate and color).
10 Selected Topics in Pediatrics for Practitioners

Steps in Resuscitation (When Liquor is not Meconium Stained)

1. Observe universal precautions like wearing gloves, cap and mask.
2. Receive in a warm towel and keep under radiant warmer
3. Positioning—slight extension of neck by keeping a rolled towel
under shoulders.
4. Clear airway—suction mouth, oropharynx and nose in that order
using a bulb syringe or suction catheter.
5. Dry, stimulate reposition give O2—Drying the newborn itself may
stimulate breathing. Back can be rubbed 3 or 4 times or gentle
flicking of sole of test to stimulate.

Fig. 2.3: Gentle stimulation to breathe

If the newborn is breathing spontaneously but has central cyanosis

administer 100 percent oxygen close to the baby’s nose.
6. Continuous evaluation every 30 seconds for respiration, heart rate
and colour.
7. Bag mask ventilation—if the newborn is still not breathing or
gasping, heart rate is less than 100 bpm or is cyanotic despite 100
percent oxygen provide positive pressure ventilation with bag-
mask. The mask should fit snugly on the face covering the nose
and mouth.
8. Oxygen is attached to the bag at a flow rate of 10 litres/minute. A
reservoir bag attached to mask will increase oxygen concentration
delivered to the baby to 90-100 percent.
 Essential Newborn Care 11

9. If supplemental oxygen is not available, continue positive pressure

ventilation using room air.
10. Adequacy of ventilation is denoted by a gentle chest rise. Majority
of babies can be resuscitated with just bag-mask ventilation.
11. If the baby fails to improve and heart rate remains < 80 bpm (beats
per minute) endotracheal intubation is mandatory if expertise is
available.
12. Chest compression
— Indication HR < 60 bpm despite 30 seconds of effective venti-
lation.
— Thumb technique Encircle chest with both hands and place
thumbs on the sternum and fingers under the chest. Apply
rhythmic sternal compression with both thumbs.
— Two finger techniques Middle and index finger perpendicularly
particularly over sternum and compress use other hand to
support newborn’s back (Figs 2.4A and B to 2.5).

One over the other Side by side

Fig. 2.4A and B: Thumb method Fig. 2.5: Two finger method

— Depth of compression: Approximately 1/3 of anteroposterior

diameter of chest.
— Coordinate with ventilation; 3 compressions followed by one
ventilation.
13. Drugs
— If HR < 60 bpm despite adequate ventilation and compression
— Epinephrine (Adrenaline) 0.5 ml 1:10000 solution through an
umbilical vein or through endotracheal tube.
— Can be repeated every 5 minutes if not improving
— Normal saline 10 ml/kg the umbilical vein if in shock.
— Sodabicarb not indicated for brief resuscitation.
Sodabicarb may be administered when other therapies are
ineffective and resuscitation is prolonged. 2 ml/kg of 4.2 percent
sodabicarb (0.5 mE/ml) administered IV over 2 minutes after
12 Selected Topics in Pediatrics for Practitioners

ensuring adequate ventilation. Avoid sodabicarb bolus in

preterm babies.
14. Resuscitation may have to be stopped if there is no sign of life after
10 minutes of CPR

Fig. 2.6: Steps in resuscitation

Post Resuscitation Care

• Continue observation in special units
• Stomach wash with normal saline (NS)
• Give vitamin K 1 mg IM
• Prevent hypothermia
• Maintenance IV fluid in the form of 10 percent dextrose.
• If in shock NS at a rate of 10 ml/kg
• Dopamine infusion at 5-10 mcg/kg/min if shock persists.
• Monitor closely for various organ function (Cardiac, renal, etc.)
• Anticonvulsants if child develops seizures.
 Essential Newborn Care 13

Fig. 2.7: Inverted pyramid of relative frequencies of

resuscitation interventions in newborn

Treatment of Neonatal Seizures

• Maintain airway and adequate ventilation
• Give phenobarbitone IV as the first drug for neonatal seizures—20
mg/kg/IV over 10 to 15 minutes; repeat 10 mg/kg if needed.
• Watch for apnea and support ventilation
• If hypoglycemia is present or suspected 2-4 ml/kg of 10 percent
dextrose IV
• If seizures persist, IV phenytoin 15 mg/kg over 10 to 15 minutes;
repeat 10 mg/kg if needed.
• Phenobarbitone and/or phenytoin are given at a maintenance dose
of 5 mg/kg/day oral or IV.

Resuscitation in Presence of Meconium Stained Liquor

Meconium stained amniotic fluid is a risk for meconium aspiration
syndrome (MAS) characterized by respiratory distress and hypoxia.
Suction mouth, nasopharynx and nares with a bulb syringe or catheter
after delivery of head and before delivery of shoulders.
If the newborn is vigorous continue initial steps of resuscitation as
for a normal newborn.
If the newborn is depressed (weak or absent respiratory effort, poor
muscle tone, HR < 100 bpm) suction the trachea through an endobronchial
tube (intubate and suction).
After clearing meconium, other steps of resuscitation are continued.
14 Selected Topics in Pediatrics for Practitioners

Meconium stained liquor/vigorous baby

Yes No

• Resuscitation stepwise like normal baby • Suction mouth and trachea

— Clear airway • Continue with resuscitation
— Dry, stimulate, reposition
— O2 as necessary

NEWBORN CARE AT DELIVERY—COMMUNITY LEVEL

Even today majority of deliveries in rural India take place at home
supervised by trained or untrained birth attendants. These people should
be taught the 5C’s to be observed during delivery, methods to keep the
baby warm, promotion of early breastfeeding and identification of high-
risk newborns and referral to a health facility with newborn unit.
Indications for Referral to a Newborn Unit
1. Preterm babies—gestational age < 36 weeks
2. Birth weight < 2000 grams
3. Severe birth asphyxia
4. Gross congenital anomalies
5. Respiratory distress or any other significant problem.
Routine Care of Newborn Immediately after Delivery at Home
The important aspects of newborn care are:
1. Provision of warmth and prevention of hypothermia
2. Breastfeeding
3. Prevention of sepsis
4. Identification of serious problem and referral if needed.
Warmth: Provision of warmth and prevention of heat loss are important
components in care of new born.
Hypothermia in the newborn is due to lack of knowledge than to lack of
equipment

Fig. 2.8: Methods of heat loss in newborn

 Essential Newborn Care 15

Figs 2.9A and B: Identification of hypothermia by touch

Fig. 2.10: Warm chain

Babies at Risk for Hypothermia

1. Preterms
2. LBW babies
3. Asphyxiated babies
4. Sick babies
5. During transport
In preterms or LBWs extraheat may be provided by skin to skin
contact (Kangaroo mother care) or overhead light source.
Kangaroo Mother Care
• Place the baby naked with nappy and a cap, upright in between
mother’s breasts.
• Let the baby suckle at breast as often as he wants
• Sleep propped up so that baby stays upright
• Even if the mother is hospitalized or wants to rest, let father or
another family member provide kangaroo care.
16 Selected Topics in Pediatrics for Practitioners

Breastfeeding
1. Keep the newborn bedded in with the mother
2. Start breastfeeding within half hour of normal delivery.
3. Colostrum is the milk secreted in the first week after delivery. It is
extremely important for the newborn as it is rich in antiinfective
factors.
4. Ensure exclusive breastfeeding during first six months of life.
Additional water is not necessary.
5. Breastfeeding technique
a. Positioning: Good positioning is recognized by the following signs
• Infant’s neck is straight or bent slightly back
• Infant’s body is turned towards the mother
• Infant’s body is close to the mother
• Infant’s whole body is supported
b. Attachment
• Chin touching breast
• Mouth wide open
• Lower lip turned outward
• More areola visible above than below the mouth

Figs 2. 11A and B: Positioning the baby for breastfeeding

(A) Correct positioning, (B) Incorrect positioning

Fig. 2.12: Attachment at breast

 Essential Newborn Care 17
6. Explain to mother and relatives about the relatively less volume of
lactation for first 3 days after delivery and reassure them about the
adequacy of this volume for the newborn. Later, adequacy of
breastfeeding is indicated by good sleep, adequate urine output (>
6 times per day) and weight gain.
7. Problems in breastfeeding and possible solutions:
• Retracted nipple—Manual stretching out, plastic syringe to draw
out the nipple (Inverted syringe technique)

Fig. 2.13: Inverted syringe technique for retracted nipple

• Breast engorgement—Early and frequent feeds; correct attachment

to breast; analgesics to mother.
• Sore nipples—Proper positioning and latching of baby to breast
• Not enough milk—Reassurance
• Working mother—Expressed breast milk

D
A

C B

Figs 2.14A D: Manual expression of breast milk

18 Selected Topics in Pediatrics for Practitioners

Prevention of Infection
a. Umbilical cord care:
— Keep cord clean and dry
— Do not apply anything over cord
— Cord may fall after 5-10 days
It may take longer if it gets infected or in immunocompromized
babies.
b. Skin care:
• Postpone bath to one day after delivery
• Look for any skin infection such as pustules or pyoderma
• Use mild unmedicated soap and warm water for bath
• Application of talcum powder is not essential.
c. Eye care: Eyes cleaned at birth and daily using sterile cotton swabs
soaked in sterile water.
d. General care: Mother should take bath and keep herself clean. Avoid
visitors and many people handling the baby.

Early Detection of Serious Problem

The following danger signs to suspect serious problem and to treat or
refer the newborn.
1. Poor feeding
2. Poor activity
3. Persistent vomiting, choking during feeding
4. Respiratory difficulty, apnea
5. Cyanosis
6. Seizures
7. Bleeding from any site
8. Jaundice within 24 hours of age, deep jaundice (involving palms
and soles), persistence of jaundice for more than 14 days of age.
9. Hypothermia, fever
10. Failure to pass meconium within 24 hours or urine within 48 hours.

Common Problems in the Newborn

Most of the problems reported in the newborn period are minor in
nature and self-limiting. Whenever a problem is reported, complete
evaluation of newborn is carried out and mother is reassured if baby is
normal.
Vomiting This is usually due to faulty feeding technique. Correct feeding
technique and burping are taught. If vomiting is persistent, bite stained
or associated with abdominal distension, intestinal obstruction should
be suspected and referred to surgeon. Vomiting may also occur due to
 Essential Newborn Care 19

any systemic disease or metabolic problem. Persistent non-bilious

vomiting after 2 to 3 weeks of birth with loss of weight should make
one suspect idiopathic hypertrophic pyloric stenosis. If it is only
regurgitation, child usually appears healthy and gains weight adequately.
Failure to pass urine All babies should pass urine within 48 hours after
birth. If not, suspect obstructive uropathy. Some normal babies may cry
before voiding. But the urine stream should be good and there should
not be any dribbling.
Diarrhoea Many newborns pass stools while being fed or soon after
feeding due to exaggerated gastrocolic reflex. These babies are active
and gain weight adequately. In exclusively breastfed babies the risk of
infective diarrhea is practically nil.
Breast engorgement Breast engorgement may be seen in both male and
female newborns in the first few days of life due to maternal hormones.
Reassurance and noninterference are indicated.
Vaginal bleeding and discharge Mild menstrual like bleeding can occur in
some female babies 3-5 days after birth lasting for 2-4 days, due to the
effect of maternal hormones. Mucoid vaginal discharge also can occur
in female newborns. Reassurance is all that is required.
Erythema toxicum Erythematous rash with central pallor appearing on
second or third day in term babies, disappears after 2-3 days without
any treatment. This is probably allergic in etiology does not require
antibiotics or antihistamines.
Umbilical granuloma A small flesh like nodule seen after the fall of
umbilical cord with persistent discharge. Cauterization with silver nitrate,
copper sulphate or common salt application is done.
Milia Yellowish white spots on the nose due to retention of sebum.
Mongolian spots Blue patches of pigmentation over sacral region and
back; disappear by 6 months of life.
Subconjunctival hemorrhages Seen in normal newborns; get absorbed
spontaneously.
Congenital teeth (natal teeth) They may be removed if they are loose to
prevent aspiration.

MANAGEMENT OF LOWBIRTH WEIGHT

(PRETERM AND IUGR) BABIES
30 to 40 percent of babies born in our country are of low birth weight
(LBW), i.e. less than 2500 grams. Among them nearly two third are due
to intrauterine growth retardation (IUGR) and born small for gestational
age (SGA).
20 Selected Topics in Pediatrics for Practitioners

LBW is of 2 types:
1. Preterm
2. IUGR (SGA)
Sometimes a combination of preterm and SGA also may be seen.

Recognition of Preterm and SGA Babies

Preterm baby
1. Skin thin, gelatinous, may appear red
2. Deep skin creases only upto anterior 1/3 of sole or absent
3. External ears-no instant recoil on folding
4. In male babies, scrotum is small with decreased rugosity and
pigmentation. Testes may be undescended.
5. In female babies, labia majora widely separated with prominent labia
minora and clitoris.

SGA Baby
1. Emaciated appearance and loose skin folds especially over thighs
and buttocks.
2. Alert look
3. Head circumference exceeds chest circumference by more than 3 cms
(normal < 2 cms)
4. Weight below 10th percentile for gestational age
Malnutrition or other adverse factors to fetus in first trimester will
result in reduction in number of cells. If chronic inadequate nutrition is
present in later pregnancy cells may be less in size, but normal in number.
If the insult to the fetus operates throughout pregnancy both number
and size of cells will be reduced.

SGA Infants are Predisposed to the Following

1. More prone for fetal distress, birth asphyxia, meconium stained liquor
and associated complications
2. Hypothermia-lack of brown fat
3. Hypoglycemia
4. Sepsis
5. Congenital malformations

Preterm Babies have the Following Risks

1. Respiratory distress—surfactant deficiency
2. Hypothermia-body surface area, brown fat, immature CNS control
3. Hypoglycemia and hypocalcemia
 Essential Newborn Care 21

Fig. 2.15: Classification based on birth weight and gestation

4. Neurologic problems—poor reflexes, intraventricular hemorrhage

5. Increased infections—defective humoral and cellular immunity
6. Anemia, hyperbilirubinemia—risk for bilirubin encephalopathy
7. Neonatal necrotizing enterocolitis (NNEC)
8. Feeding problems—gastroesophageal reflux, ileus.
9. Fluid and electrolyte problems due to glomerular filtration rate and
immature kidneys

Management of LBW Babies (Preterm and SGA Babies)

Delivery
• Early referral if LBW baby anticipated
• Preparation and resuscitation similar to term babies
• Provision of warmth and prevention of hypothermia is a priority.
Use warmer or a overhead 200 watt bulb. Use Kangaroo mother care
(KMC) to prevent hypothermia.
22 Selected Topics in Pediatrics for Practitioners

Newborn Period
• Continue to keep the child warm by wrapping in 2 to 3 layers of
cloth and keeping close to mother
• May require oxygen therapy and assisted ventilation for respiratory
distress
• Fluid and electrolyte maintenance
• Hyperbilirubinemia—phototherapy
• Feeding—direct breastfeeds if baby > 36 weeks and active with good
reflexes. Expressed breast milk through paladai after stabilizing the
child. Many healthy LBW babies < 34 weeks will need NG feeding
(EBM) initially. Gradually change to paladai feeds and later direct
breastfeeding. Very sick LBW babies require intravenous fluids.

Follow up
• At discharge baby should be maintaining temperature, taking feeds
and gaining weight
• Mother counseled adequately on maintenance of warmth, exclusive
breast feeding, prevention of infection and danger signs to bring the
baby back
• During follow up, weight and breastfeeding assessed.
• Immunization as per schedule
• Eye check up (for ROP), hearing and neurologic assessment

Home Care for Preterm and SGA Babies

Most healthy newborn with a birth weight > 1800 grams and gest age
of > 35 weeks can be managed at home with maintenance of warmth,
breast feeding (some may need EBM through paladai initially) and
prevention of infection. They need more frequent weighing and follow
up.

JAUNDICE IN NEWBORN
About 60 percent of term infants and 80 percent of preterm infants
develop some degree of jaundice during first week of life.

Assessment of Jaundice
Clinical
• Look at skin colour from face downwards
• Blanch the skin and then look at underlying skin colour
• Extent of jaundice is a rough estimate of serum bilirubin
 Essential Newborn Care 23

Laboratory: Assessment of serum bilirubin

Clinical Criteria to Assess Jaundice

Body area Bilirubin (mg/dl)
Face 4
Upper trunk 5-12
Lower trunk and thighs 8-16
Arms and lower legs 11-18
Palms and soles > 15

Bilirubin Encephalopathy
High levels of unconjugated bilirubin can cause toxic neuronal drainage
in the brain.
• Physiological jaundice
• Appears between 24-72 hours of age
• Maximum intensity 4-5 days in term; disappears by 10th day of life
• Does not exceed 15 mg/dl
• Not detectable clinically after 14 days of life
Baby observed for any increase in jaundice; no treatment needed.

Pathological Jaundice
• Jaundice appearing within first 24 hours after birth
• Serum bilirubin > 15 mg/dl
• Clinical jaundice persisting > 14 days of life
• Stool clay/white colored with dark yellow urine.
One should try to find out the cause of pathological hyperbiliru-
binemia. Treatment is needed in the form of phototherapy or exchange
transfusion.

Causes of Jaundice
Appearing Within First 24 hours of Age
• Hemolytic disease of newborn: Rh, ABO incompatibility
• Infections: Intrauterine, viral, bacterial
• G-6 PD deficiency

Appearing at 24-72 Hours of Age

• Physiological jaundice
• Neonatal sepsis
• Concealed hemorrhages: Cephalhematoma
• Polycythemia
• Mild hemolytic states
24 Selected Topics in Pediatrics for Practitioners

Appearing After 72 Hours of Age

• Neonatal sepsis
• Neonatal hepatitis
• Extrahepatic biliary atresia
• Breast milk jaundice
• Metabolic disorders such as galactosemia
Infection must be ruled out in jaundice appearing anytime after third
day of life

Breast Milk Jaundice

• May appear after 3rd day and present as prolonged physiological
jaundice
• Child is active feeds well and no sign of any other illness seen
• Frequent breastfeeding without interruption —jaundice spontaneously
settles.

Management of Neonatal Jaundice

Reduction of unconjugated bilirubin—by phototherapy and exchange
transfusion. Early and frequent breast feeding is ensured.
• Mild jaundice (Bilirubin 5-12 mg/dl): Observation and follow up
• Moderate (13-17 mg/dl) : Phototherapy
Blood groups of mother and baby
Periodic bilirubin measurement
• Severe (> 18 mg/dl) : Phototherapy immediately
20-25 mg: investigate, continue
phototherapy and prepare for exchange
transfusion
> 25 mg: Exchange transfusion
If the newborn is preterm, had asphyxia or is sick, treat as for a lower
range of bilirubin.

Phototherapy
• Exposure of naked newborn to blue or white fluorescent light at
wavelength of 450-460 mm
• Bilirubin is converted to nontoxic soluble forms and excreted
• Frequent feeding and change of posture of baby
• Baby is placed naked 45 cm from tube lights on a crib or incubator
• Eyes and gonads covered
• Discontinue if 2 bilirubin values < 10 mg/dl
 Essential Newborn Care 25

Exchange Transfusion
Most effective and reliable method to reduce bilirubin
• In ABO incompatibility: Emergency O +ve blood;
— Ideal O +ve suspended in AB plasma
• In Rh incompatibility: Emergency O –ve blood;
— Ideal O –ve suspended in AB plasma;
— Baby group Rh-ve is other alternative
• Other conditions: Baby’s blood group

RESPIRATORY DISTRESS IN NEW BORN

Respiratory distress is indicated by:
• Respirate rate > 60/minute when the baby is quiet.
• Indrawing of intercostal spaces and sternum at nasal flaring during
inspiration
• Expiratory grunt
• Central cyanosis

Causes
1. Pneumonia—by gram-negative organisms from maternal genital tract.
2. Transient tachypnoea of newborn (TTN)—more common in term
babies and those born by LSCS
3. Meconium aspiration syndrome (MAS)—often associated with birth
asphyxia and post maturity
4. Hyaline membrane disease (HMD)—surfactant deficiency mostly in
preterm babies.
5. Congenital malformations—like diaphragmatic hernia, oesophageal
atresia with tracheo-oesophageal fistula.

General Management Principles

1. Oxygen administration
• For mild respiratory distress—O2 through nasal cannula (0.5 to
2.0 L/min)
• Moderate to severe distress—by oxyhood (1-5 L/min)
• In conditions like HMD and MAS ventilatory support in neonatal
units often needed
2. Keep the baby warm
3. Antibiotic therapy—for suspected pneumonia. Gentamycin plus
penicillin or ampicillin IV or IM
4. Fluids and feeds
• NGT feeds for those babies with mild to moderate distress
• Severe respiratory distress, sick child: IV fluids
26 Selected Topics in Pediatrics for Practitioners

5. Take a chest X-ray

6. Keep monitoring till child stabilizes—respiratory rate, HR, perfusion,
oxygen saturation

NEONATAL SEPSIS
Neonatal sepsis is a clinical syndrome of bacteremia with systemic signs
and symptoms of infection in the neonatal period (first four weeks of
life). It can be a generalized infection such as septicemia or may be a
localized deep-seated infection such as pneumonia or meningitis.
Neonatal sepsis is the most important cause of neonatal deaths in our
country accounting for more than half of them. Low birth weight is an
important underlying condition.

Early Onset Neonatal Sepsis

• Onset of symptoms during first 72 hours of life.
• Caused by organisms from maternal genital tract such as E coli.
• Frequently manifests as pneumonia: Less commonly as sepsis or
meningitis.
• Predisposing factors—prolonged rupture of membranes (> 24 hours),
prolonged labor, maternal fever and aspiration of meconium.

Late Onset Sepsis

• Onset after 72 hours of birth
• Caused by organisms in the external environments of home or hospital
• Staphylococcus and klebsiella.
• Manifests as septicemia, pneumonia or meningitis.
• Predisposing factors: Lack of breastfeeds, superficial infections (pustu-
les, umbilical sepsis), use of intravenous lines or other invasive
procedures in hospital.

Clinical Features
• Clinical manifestations are often vague and nonspecific.
• Alteration in feeding pattern such as refusal to feed is the most
characteristic early feature
• Lethargy, activity, responsiveness
• Hypothermia, fever
• Vomiting, abdominal distension
• Tachypnea, chest retractions, apnea
• Vacant look, seizures
• Cyanosis, jaundice, pallor
• Shock, sclerema.
 Essential Newborn Care 27

Diagnosis
1. Blood, CSF and urine culture
2. Leukopenia (Total count < 5000/cmm), immature to total neutrophil
ratio > 0.2, micro ESR > 15 mm/1st hour and CRP positivity (> 8 mg/
ml) are useful indirect methods to diagnose sepsis.
3. Chest X-ray—look for pneumonia

Treatment
• Do not delay specific therapy in obvious cases of sepsis
• Early treatment is crucial

Specific Therapy
Usually a combination of ampicillin or benzyl penicillin with gentamycin
for community acquired sepsis.

Supportive Therapy
• Keep the baby worm
• Intravenous fluids
• If perfusion is poor, give normal saline 10 ml/kg over 10 minutes;
this can be repeated once or twice if poor perfusion persists.
• Give oxygen and support ventilation as needed.

Prevention of Infections
1. Hand washing
• All persons handling newborns should strictly follow hand
washing before touching any baby.
• Wash hands upto elbows with a thorough scrub for 2 minutes
with soap and water. Rinse thoroughly under running water.
• Dry hands with sterile towel/paper towel
• Wash hands for 10 seconds in between patients
2. Cord care: Umbilical cord is left clean and dry
3. Use disposable items for invasive and non-invasive interventions.
4. Early treatment of superficial infection
• Superficial infections like pustules and umbilical sepsis are
adequately managed, otherwise they may lead onto sepsis
• Local application of 0.5 percent gentian violet and oral antibiotics
like amoxycillin or cotrimaxafole (avoid in premature babies and
jaundiced babies) is effective

TRANSPORT OF NEONATAL
• In utero transport of pregnant woman when risk is anticipated, is
more optimal
28 Selected Topics in Pediatrics for Practitioners

• When this is not possible, babies with problems may have to be

transported to higher centers, after delivery.
• Transport should be done in an efficient manner

Preparation for Transport

• Communicate with parents: Need and place of transport
• Correct hypothermia
• Clear airway, maintain respiration, O2 if needed
• EBM or breastfeed if possible
• Prepare a note if child’s condition and drugs given
• Encourage mother to accompany baby to continue breastfeeding and
provide warmth (KMC)
• Arrange for a health care provider to accompany the baby
• Communicate to the center where baby is being referred

Provision of Warm Transport

• Skin to skin care (KMC)
• Cover the baby with clothes and keep close to mother
• Thermocool box, polythene cover or cotton padding used for
maintenance of warmth

Provision of Other Care During Transport

• Maintain airway, breathing
• O2 if needed
• Breastfeed or EBM through paladai if possible, otherwise EBM
through NG tube enroute.

BIBLIOGRAPHY
1. Cloherty JP, Stark AR. Manual of neonatal care (3rd edn). Little Brown: Boston
1991.
2. Neonatal resuscitation. In PALS provider manual, American Heart Association,
2002 guidelines.
3. Singh M. Care of newborn (5th edn). Sagar Publication: New Delhi, 1999.
 3
Practical Aspects of
Growth and Development
in Early Childhood
S Thangavelu

During the routine well child visits in the first year life, every pediatrician
has got five responsibilities.
1. Growth monitoring
2. Developmental assessment
3. Immunization
4. Advice on nutrition and child safety
5. Examination and identification of an asymptomatic diseases such as
congenital heart disease
Growth is defined as increase in size and development is functional
maturity. It is gradual acquisition of learned skills from a state of helpless
neonate to a fully independent adult

GROWTH MONITORING
Aim of growth monitoring is early identification of abnormal deviation
growth either upward or downward. There are many methods available
to monitor growth
1. Anthropometry
2. Skeletal assessment
3. Tissue growth assessment—skin fold thickness
4. Dental development
Among this anthropometry is the practically useful one and some
times skeletal and tissue growth assessments are useful.
1. Weight Though beam type weighing machines are preferable than
spring type, later is widely used because of low cost and availability.
But spring type machines should be frequently checked for error and
if needed to be changed to a fresh one. Check for zero error. Use
minimum clothes for the baby. Weigh with 50 gram accuracy. When
the child is holding on to nearby surface weight recorded will be too
low.
30 Selected Topics in Pediatrics for Practitioners

2. Length Till the age of 2 years, recumbent length is measured with

either infantometer or simply using two wooden blocks on head and
foot ends.
After 3 years child may cooperate with the examiner to measure
height either with stadiometer or by using a tape fixed in wall. Other
anthropometric measurements, which are useful are
1. Mid-arm medium circumference One of the very useful measurement
for field studies. This is one of the age independent variable as MAC
is relatively constant between 1-5 years. Any measurement less than
12.5 cm indicates malnutrition and above 13.5 cm is considered as
normal.
2. Body mass index (BMI)
Weight (kg)
BMI = ______________________
Height2 (m)
BMI of more than 30 needs, evaluation for obesity
3. Triceps skin fold thickness Measurement of Triceps skin fold thickness
and subscapular skin fold thickness are indices of adiposity.
4. Body proportion Body proportion is assessed by measuring the lower
body segment from symphysis pubis to the floor. By deducting this
from height of the child upper body segment is calculated. The ratio
of US/LS ratio equals 1.7 at birth, 1.3 at 3 years 1.0 at 7 years. Higher
US/LS ratio indicate short limbs.

Interpretation by Comparing with Age Appropriate Values

Interpretation is done by comparing with reference standards or by
plotting in the growth charts. In this method, measured values of the
child is compared with the reference standards or expected height and
weight for that age. There are formula or rule of thumb for each
measurement.
Height
At birth 50 cm
At 1 year 75 cm
2-12 years (age in years × 6) + 77

Weight
At birth 3.00 kg
3-12 months Age in mo + 9/2
1-6 years (Age in years × 2) + 8
(Age in years × 7) – 5
______________________________
7-12 years
2
 Practical Aspects of Growth and Development in Early Childhood 31

Head Circumference
At birth 32-35 cm
Gain in first 3 months 3 × 2 = 6 cm
4-6 months 3 × 1 = 3 cm
7-12 months 6 × ½ = 3 cm
At 1 year 45-46 cm
2 years 47 cm
3 years 48 cm
4 years 49 cm
5 years 50 cm
Comparing the patient values with reference standard, various
classifications such as IAP classification and welcome classification have
graded the malnutrition. Correct method of height measurement is shown
in picture.

Head Circumference
It is mandatory to record head circumference in the first 3 years of life
non-stretchable tape should be used, encircling the head above the
eyebrows and over occiput

Chest Circumference
It should be measured at the level of xiphoid. Before one year of age
head circumference is more than that of chest circumference. At one year
of age both are equal and beyond one year chest circumference starts
increasing than the head circumference.

Recording
Measurement should be recorded both in units as well as in percentiles.
It is essential to record the date.

Interpretation by Plotting in the Growth Charts

Interpretation is done commonly using the standard weight or height
expected for the age. Less commonly, but more precisely it is done by
plotting in the growth charts.

Growth Chart
Internationally accepted charts like NCHS growth charts can be used.
Periodically plotting the measurement will give a clear idea of growth
pattern. Following procedure is adopted to plot the height in the growth
chart.
32 Selected Topics in Pediatrics for Practitioners

1. First calculate the midparental height by adding heights of father

and mother and divide by two. For boys 7 cm is added; for girls 7
cm is subtracted
E.g. Father’s height 170 cm
Mother’s height 158 cm
170+158
_______________
Average is = = 164 cm
2
For boys add 7 hence 164 + 7 = 171 cm
For girls subtract hence 164 – 7 = 154 cm
2. Plot the mid parental height on centile chart at the age of 19 years
3. If the child is 10 years old and the child’s height is 125 cm. This is
plotted in the chart. This centile line is followed up to the age of 19
years on the chart
4. If the child’s centile at 19 year is within 8.5 cm for girls and 10 cm
for boys of the mid parental height, then considered compatible with
that of parents.

What is Abnormal and Needs Further Investigations

1. Children having measurements less than 3rd percentile and more
than 97th percentile.
2. Children crossing 2 centile lines.

IAP (Indian Academy of Pediatrics) Classification

Nutritional grade % age of standard weight for
Normal More than 80% age
Grade I 71-80%
Grade II 61-70%
Grade III 51-60%
Grade IV 50 or less than 50%

Welcome Classification
% of the reference weight Edema
Normal > 80% - No
Under nutrition 61-80% - No
Kwashiorkor 60-80% +
Marasmus < 60% No
Marasmic Kwashiorkor < 60% +

Growth Velocity
Growth for example, height is measured in an interval of at least 6
months. The calculated for an year and plotted in the chart. A velocity
below the 50th percentiles means that the child is progressively deviating
from the normal growth.
 Practical Aspects of Growth and Development in Early Childhood 33

Causes of Growth Delay

Any child’s height falls below 3rd percentile is considered as short.
Non-pathological causes are excluded first.
1. Familial short stature Usually a well child without any dysmorphic
facies. Height percentile is compatible with midparental height. In a
growth chart, child’s growth will not fall and cross the centiles.
Inherited causes of short stature such as rare causes of growth
hormone deficiency should not be missed.
2. Constitutional growth delay and puberty This is more commonly seen
in boys than girls. These children will continue to grow into late teen
age. There will be family history of delayed growth and late puberty.
They will be short in the late years of first decade and early teens.
No adolescent growth spurt observed. Bone age will correspond to
the height, but will be delayed for actual age. Ultimately they will
achieve the normal growth potential.
If these two causes are excluded, rest of them can be categorized into
four groups based on height and build or weight percentile.
1. Short and fat child Apart from endocrine causes children with
psychosocial deprivation also present in this manners. Hypothy-
roidism, hypopituitarism, Cushing’s syndrome and pseudo-
hypoparathyroidism are the endocrine causes.
2. Short and thin or normal child Children with chronic systemic diseases,
malabsorption, some of the low birth weight children and children
with psychosocial deprivation are short and thin.
3. Disproportionate short stature Skeletal abnormality like achondroplasia,
systemic metabolic disorders like mucopolysaccharidosis and
untreated congenital hypothyroidism belong to this group.
4. Short child with dysmorphic features Chromosomal abnormalities like
Down’s syndrome, Turner’s syndrome and others like Prader-Willi
syndrome are some of the causes.

Evaluation
History
• Birth weight, serious events in the medical history.
• Family history of delayed puberty-parental height and height of
siblings.
• Any systemic illness with special reference to appetite, recurrent or
chronic infection, chronic respiratory and gastrointestinal problems
or renal disease.
• History of contact—tuberculosis, HIV
• Adverse social history or emotional deprivation.
34 Selected Topics in Pediatrics for Practitioners

Examination
• Complete anthropometry
• Signs of undernutrition—pallor, vitamin A, D deficiency
• Abnormal facies
• Skeletal deformity and disproportion
• Signs of chronic systemic illness—clubbing, cyanosis, organomegaly.

Investigation
• Complete blood count
• Mantoux, HIV screening, chest X-ray
• Electrolyte, calcium, urea, creatinine
• Thyroid function tests
• Chromasomal study.

DEVELOPMENTAL ASSESSMENT
Development is a mini replay of what happened in the tree of evolution.
It took 25 million years for the walking human race to evolve from a life
started with a monocellular organism in this earth. It is fascinating to
know that individual human life also starts as monocellular zygote.
After spending 10 months antenatally and 15 months postnatally, at the
end of 25 months a child starts walking. 25 million years of evolution
is compressed in 25 months during development.
If various achievements and special capabilities of human race are
compared with development of a child, they are interestingly comparable.

Biological achievements of human race Equivalent achievements in the

which is different from other animals development of an infant

1. His upright posture and 1. Gross motor involving body posture and large
locomotion with legs leaving movements
his hands free for more precise
activities
2. Finely adjustable visual 2. Fine movement of fingers, guided by vision to
equipment and uniquely flexible develop manipulative skills
digit from what best of human
discoveries originated

3. Possession of spoken language 3. Hearing and speech

4. Evolution of complex social culture 4. Social behavior and spontaneous play involving
for the protection of young and organization of self with gradual acceptance of
rescue of elderly social standards with regarding to personal
relationship and cultural demands
 Practical Aspects of Growth and Development in Early Childhood 35

Basic physical needs of a child are comprised of shelter and protective

care, food, clothing, fresh air and sunlight, activity and rest, training in
habits and skills necessary to sustain life. Basic psychological needs
which are essential for emotional and intellectual development are
affection and continuity of individual care, security, sense of personal
identity and self respect, opportunity to learn from experience, opportu-
nity to achieve success, achieve independence and to take responsibility
and to be of service to others.

Common Presentation of a Developmental Disability

Failure to achieve the age appropriate developmental skills is the common
way of presentation.
In the first 6 months of life—poor suck, floppy or spastic tone, lack
of social smile or startle indicates abnormal development Later months
of first year—delay in sitting, crawling and standing suggest delay in
motor development. Second and third year of life—Language and beha-
vioral abnormalities point to developmental delay. In the school age—
attention deficit and hyperactivity disorders are identified in this age.
36 Selected Topics in Pediatrics for Practitioners

Identification of Developmental Delay

This is done by three part evaluation.
1. Developmental history
2. Physical and neurological examination
3. Developmental screening.

Developmental History
This includes an organized way of tracking developmental milestones
during every visit in a chronological order. Development quotient (DQ)
can be calculated by this:
Functional age
_______________________
DQ = × 100
Chronological age
E.g. 12 months old child just starts sitting up
7 months (usual age for sitting)
12 months (sitting achieved by child)
60% (approximate)

Physical Examination
Growth Parameter
• Microcephaly, macrocephaly, short stature
• Congenital abnormalities
• CHD, cleft palate may be associated with systemic disease
• Major anomalies suggest a syndrome with mental retardation as a
component
• Orthopedic anomalies—contractures, motor impairment may be a
part of the syndrome.
• Skin—neurocutaneous markers
• Organomegaly—neurometabolic disorder.

Neurological Examination
Apart from classical neurological examination, asymmetry of power,
muscle tone and deep tendon reflexes, postural response and primitive
reflexes are to be looked for.

Developmental Screening
As a busy pediatrician cannot spend more time in developmental
assessment, they can use simple screening scales, which will not consume
more than 5 or 10 minutes. Ideal time is when the child is neither
hungry nor sleepy after feeds. He should not be sick or irritable or
uncooperative. One of the following methods can be used.
 Practical Aspects of Growth and Development in Early Childhood 37

1. Trivandrum developmental scale (TDS)

2. Developmental screening scale designed by S Lingam used by health
workers and physician in United Kingdom.

TDS
This test is developed in Trivandrum, comprising of 17 test items, which
is assessed according to the age of the child, e.g. Keep a pen vertically
over the chronological age. All the skills on the left side, a child must
be able to achieve. At a glance one can decide whether there is
developmental delay.

Developmental Screening Chart (S Lingam 1987)

This chart describes the appropriate skills attained at various ages from
6 weeks to 3 years. These are classified individually as gross motor, fine
motor, social and language. Hence, delay in individual aspects of
milestone can be precisely identified. It is administered using simple
tools like a bright object (red woolen balls) rattles, cup and spoon, bell,
one inch square bricks in four colors, pencil and paper, small objects like
dry grapes or puffed rice. Skills are recognized by history from parents,
as some children may fail to perform the task even though they can, in
the presence of the strangers

General Rules of Developmental Assessment

1. It is easier to observe the child during its activity and play rather
than directly administering the task or skill.
2. Never separate the child from the mother for the sake of
developmental assessment. It can be performed by keeping the child
in mother’s lap.
3. During assessment start from the non-invasive to invasive ways of
assessment. Begin in the order—social, language, fine motor and
finally gross motor assessment. If gross motor assessment is done in
the beginning by moving the limbs, child may start crying and may
not cooperate for rest of the assessment.
4. At the end of the assessment if the inference is doubtful or the child
fails to cooperate repeat the test at some other time rather than
giving a comment about the assessment.
5. If the child is consistently failing the test and the suspicion of
developmental delay is stronger, then the child may be referred to
a developmental pediatric team for the detailed assessment and
remediation.
6. When a preterm child is assessed calculate the corrected age by
deducting the period of prematurity in the first year and half of it
in the second year.
 Developmental Screening Scale (S Lingam 1987, UK)

4-6 weeks 3 months 6 months 9 months One year 18 months 2-2½ years 3 years

Gross Supine: Supine: Supine: Sits alone Pulls to Climbs Kicks ball Running
motor head on head in Raises 10-15 stand upstairs one Jumps in and can turn
sides, midline head, lifts minutes Walks hand held place around
hands Hands legs, grasp Leans around Carries toy Climbs up obstacles
closed, open, foot forward holding on while and Can pull
thumbs in moves arm On without to furniture walking descends large toys
pulled to symmetrica grasping losing Climbs stairs with Climbs
sitting lly hand pulls balance forward into holding on stairs in
head Hands self to sit Attempts to adult chair to rail adult
momentarily together in Prone: crawl manner
erect midline hand Forward Descends
and fall pulls to support parachute two feet to a
held sitting little Sitting with (7 m) step
sitting: or no support Rolls over Jumps from
back headlag straight back to bottom step
curved Kicks back prone Walks
ventral vigorously Downward forward,
suspension: ventral parachute: backward,
38 Selected Topics in Pediatrics for Practitioners

Head in suspension bears sideward

line with Head weight on
trunk above trunk feet
Walking, Prone lifts
stepping head with
reflex forearm
support
Fine Turns Follows Moves Very Holds two Builds tower Picks up Builds tower
motor eyes and adult head and attentive bricks and with 3-4 thread of 9 cubes
head movements eyes early Visual: bangs cubes Removes One or
towards with in all Good Fine pincer Scribbling paper more

Contd...
Contd...

4-6 weeks 3 months 6 months 9 months One year 18 months 2-2½ years 3 years

light available directions peripheral grasp Turns pages wrapping bridges of 3

Shuts field Fixes eyes vision Points with in bunches from cubes
eyes to Follows ball on objects Pokes at index finger chocolate Copies
bright light ½ circle Reaches small Picks up imitates circle,
Regards hand and grasp objects raisin vertical imitates +
mother regard palmar Pincer lines Matches or
face Finger play grasp grasp Builds names 2 or
Follows Defensive Transfers Watches tower of 8 bricks 3 primary colours
ball ¼ blink object from rolling ball Turns pages Cuts with scissors
circle one hand at 10 feet singly, hand
to other preference
Language `Startle’, Quietening Turns Long Turns to Points to Refers to Gives full
stiffens or smiling immediately repetitive name eyes, nose, self by name, sex
blinks, to mother’s to mothers string of Understands mouth name and
screws up voice voice Mono syllable- simple Obeys Joins in sometimes
eyes and double Mama, instruction simple nursery age
Fan out syllable Dada with commands rhymes Many
fingers Responds to Understands gesture (close the and sings questions-
Cries or distraction no, no, (give it to door) Uses fifty What, why,
freeze in hearing bye bye daddy) Uses 6-20 words where?
response test at 1½ Hearing Two recognisable Puts two- Listens
to noise feet at ear test meaningful words three eagerly to
level response 3 words Enjoys words into stories
Laughs feet below nursery simple Carries on
and above rhymes sentences simple
Attempts to Constantly conversation
sing asking conversation
Practical Aspects of Growth and Development in Early Childhood

Contd...
39
Contd...

4-6 weeks 3 months 6 months 9 months One year 18 months 2-2½ years 3 years

and names of objects

chuckles and people
Social Turns to Fixes eyes Reach and Plays peek- Plays pat a Explores Plays Washes
regard on mother grasp small A-Boo cake environment alone pulls hands but
nearby Unblinking, toys Holds, bites Drinks from Holds and down needs
speaker’s purposeful Takes to and chews cup spoon feeds pants at supervision
face gaze mouth biscuits Waves himself toilet but Can pull
Stops Smiles, Shakes Reserved bye-bye Takes off can’t pants down
crying coos to rattle with shoes and replace and up but
when familiar Holds strangers socks Eats needs help
picked up situations bottle and (7 m) skillfully for buttoning
and feeds Imitates with spoon Shares,
spoken to Still friendly hand Little plays with
Social with clapping understand other
smile strangers Finds a toy ing of Shows
partly dangers to affection for
hidden defer younger
wishes sibling
40 Selected Topics in Pediatrics for Practitioners

Warning Not Not Persistent No hand Not starting Not moving Avoiding Not
signs for responding showing moro, transfer a variety of about to eye following
further to nearby interest in asymmetric Not sitting speech explore contact simple
evaluation voices by people/ tonic neck No sounds Not Handedness direction
8 weeks playthings reflex repetitive Not pulling Speaking before 2 Monotonous
Absent by 3-4 Not visually babble to standing single word years, Look play by self
`Startle’ months alert even by 10 position by 21 for
No social No head Not months months weakness
smile by 3 control by 5 reaching (average of opposite
months months for objects 13-15 mo) hand
No No
vocalization sentence by 27 months
 Practical Aspects of Growth and Development in Early Childhood 41

Causes of Selective Delay in Motor Milestones

1. Severe degrees of malnutrition
2. Rickets
3. Neuromuscular diseases—spinal muscular atrophy
4. Spinal cord disorders—where only lower limbs are affected

Causes of Selective Language Delay

1. There is a wide variation in achievement of skill, hence allowance
should be given till the upper limit of normal age before declaring
as delayed.
2. Always consider social deprivation as a cause of delay, e.g. A child
brought up in an orphanage.

BIBLIOGRAPHY
1. IAP Textbook of Pediatrics (2nd edn). New Delhi, 2002.
2. Indian Journal of Practical Pediatrics, 1999;1,1.
3. KE Elizabeth. Infant and child nutrition.
4. Leon Polnay. Manual of community pediatrics. Churchill Livingstone, 1996.
5. Marry D Sheridan. From Birth to Fiver years, 1975.
6. Pediatric Clinics of North America. The child with developmental disabilities.
1993;40:465-77.
7. S Lingam. Manual of child development. Churchill Livingstone, 1999.
 4
Infant and Young Child Feeding
A Parthasarathy

Breastfeeding assumes extreme and prime importance in infant and

young child feeding. Excerpts from the recent advances in breast, infant
and young child feeding are described here under to enable practitioners
of pediatrics to have first hand and updated knowledge on the subject
The IMS Act 1991 has further been modified in 2002 banning the
advertisements and free sample distribution of even infant weaning
foods.

Introduction
Doctors are important and frequent source of contact with both parents
throughout pregnancy and after birth. There are many opportunities of
educating them about successful breastfeeding in the prenatal period,
assisting during labour and immediate postnatal period. To get the best
of breastfeeding, we need to create a ‘warm-chain’ of support that is,
skilled care for mothers to build their confidence and show them what
to do and protection from harmful practices. If this ‘warm chain’ has
been lost from the culture, or is faulty, then it must be made good by
the health services.
Apart from being prepared during the medical schools, doctors also
need to be updated continuously to learn new concepts and knowledge
or new research evidence e.g. on duration of exclusive breast feeding,
everchanging scenario of breastfeeding and HIV, etc.

Definition of Infant Feeding (Table 4.1)

WHO Global Data Bank has addressed this question and the Table
below gives the definitions and explains these as well.

Benefits of Exclusive Breastfeeding

Exclusive breastfeeding implies giving newborn infants no food or drink
other than breast milk unless medically indicated. The concept of exclu-
sive breastfeeding was first introduced in 1989 by UNICEF and WHO
when a set of suggested policy statements and guidelines were issued
entitled ‘protecting, prompting and supporting breastfeeding—the special
 Infant and Young Child Feeding 43

Table 4.1
Category of Requires that Allows the infant Does not allow the
infant feeding the infant receives to receive infant to receive

Exclusive Breast milk Drops, syrups (vitamins, Anything else

breast (including milk minerals, medicines)
feeding expressed or
from wet-nurse)
Predominant Breast milk Liquids (water and Any thing else (in
breastfeeding (including milk water-based drinks particular, non-
expressed or from fruit juice, ORS), ritual human milk, food
wet-nurse) as the fluids and drops, syrups based fluids)
predominant source (vitamins minerals,
of nourishment medicines)
Complementary Breast milk and solid Any food or liquid
feeding or semi-solid food including non-human milk

Breastfeeding Breast milk Any food or liquid —

including non-human milk
Bottlefeeding Any liquid or Any food or liquid including
semi-solid food from non-human milk. Also allows
a bottle with nipple/ breast milk by bottle
teat

Table adopted from Recent Advances in Pediatrics – Special Vol II: Community Pediatrics year
2002, Breastfeeding, Arun Gupta, ed. Suraj Gupte, Jaypee Bros, New Delhi, 2002.

role of Maternity care practices were developed and published. Thereafter

exclusive breastfeeding was incorporated in various health programs
including baby friendly hospital initiative, which was launched
worldwide in 1992. Initial recommendations were exclusive breastfeeding
for first 4 –6 months of life. American Academy of Pediatrics suggested
exclusive breastfeeding for approximately the first six months. It took
more than ten years before the World Health Assembly (WHA 54:2,18
May, 2001) adopted the resolution to approve exclusive breastfeeding
for first six months. Duration of exclusive breastfeeding has become a
valid tool to assess the state of breastfeeding and appropriate intervention
in a particular community.
• Ensures intake of colostrum
• Provides optimal nutrition
• No water supplementation is required
• Reduces risk of various infectious and non-infectious diseases.
• Contributes to better intelligence
• Promotes emotional development between mother and baby.
• Prevents breast problems in mother
• Reduces risk of breast and ovarian cancer, iron deficiency anemia
and hip fracture in mother
• Helps in birth spacing.
44 Selected Topics in Pediatrics for Practitioners

Breastfeeding and Child Health

Breastfeeding confers life saving protection against various acute
childhood illnesses as well as chronic diseases. As a result breastfeeding
promotion has become an important health intervention tool in various
child health programs worldwide.
Breastfeeding provides several physical, biological and biochemical
barriers against infectious agents. It also limits exposure to environmental
pathogens that may be introduced through contaminated food or feeding
devices.

Gastrointestinal Diseases
Breastfeeding has been well documented to prevent and attenuate the
severity of diarrheal diseases in developing world and specially against
enteric pathogens such as Rotavirus, Giardia lamblia, Shigella sp.,
Campylobacter sp., and enterotoxigenic E.coli.

Practical Points for Breastfeeding

1. Start breastfeeding within ½ to 1 hour including giving colostrum.
2. The baby should be kept next to the mother in the same bed.
3. Correct positioning and attachment at the breast is essential.
4. Baby should be breastfed on demand including feeding during the
night and for as long as he/she wants. The baby should be allowed
to finish the contents of the breast first before offering the second.
5. Babies should be exclusively breastfed for four to six months, followed
by appropriate complementary feeding and continuing breastfeeding
for at least 2 years. Exclusively breastfed infants do not need water
even in hot weather.
6. More suckling makes more milk.

Breastfeeding and Mother’s Medication (Table 4.2)

Table 4.2
Breastfeeding Anticancer drugs (antimetabolites); Radioactive substances (stop
contraindicated breastfeeding temporarily)
Continue breastfeeding: Psychiatric drugs and anticonvulsants
Side-effects possible
Monitor baby for
drowsiness
Use alternative drug Chloramphenicol, tetracyclines, metronidazole, quinolone antibiotics
if possible (e.g. ciprofloxacin)
Monitor baby for Sulfonamides, dapsone
Jaundice Sulpamethoxazole + pyrimethamine (Sulfa+Pyri)

Contd...
 Infant and Young Child Feeding 45

Contd...

Use alternative drug Estrogen—containing contraceptives, thiazide diuretics, ergometrine.

(may inhibit lactation)
Safe in usual dosage Most commonly used drugs:
Monitor baby Analgesics and antipyretics: short courses of paracetamol,
acetylsalicylic acid, ibuprofen; occasional doses of morphine and
pethidine
Antibiotics: Ampicillin, amoxicillin, cloxacillin and other Penicillins,
erythromycin, Antituberculosis and antileprosy drugs Antimalarials
(except mefloquine, Sulfa+pyri) Anthelminthics Antifungals.
Bronchodilators (e.g. salbutamol, corticosteroids), Antihistamines,
antacids, drugs for diabetes, Most antihypertensives, dioxin,
Nutritional supplements of iodine, iron, vitamins

Table adopted from Recent Advances in Pediatrics – Special Vol II: Community Pediatrics year
2002, Breast feeding, Arun Gupta, Suraj Gupte (Eds), Jaypee Bros: New Delhi, 2002.

BABY FRIENDLY HOSPITAL INITIATIVE

The Baby Friendly Hospital Initiative (BFHI), was launched by WHO
and UNICEF in May 1991 for the protection, promotion and support of
successful breastfeeding. It is a significant strategy towards the
establishment of the breastfeeding culture globally and is based on the
“ten steps for successful breastfeeding”. As signatory to the Innocenti
Declaration several countries had committed to promote all maternity
health care facilities in the country into baby friendly hospital by the
year 2000. Baby friendly hospitals are hospitals that have changed their
practices to support breastfeeding, following the ten steps below.
1. Have a written breastfeeding policy that is routinely communicated
to all health care staff.
2. Train all health care staff in skills necessary to implement this
policy.
3. Inform all pregnant women about the benefits and management of
breastfeeding.
4. Help mothers initiate breastfeeding within half an hour of birth.
5. Show mothers how to maintain lactation even if they are separated
from their infants.
6. Give newborn infants no food or drink other than breast milk
unless medically indicated.
7. Practice rooming in, allow mother and infant to stay together
24 hours a day.
8. Encourage breastfeeding on demand.
9. Give no artificial feeds or pacifiers to breastfeeding infants.
10. Foster the establishment of breastfeeding support groups and refer
mothers to them on discharge from hospital or clinic.
Adopted from Shameem Ahamad. Breastfeeding revisited: RAP: Special
Vol III. In Suraj Gupte (Ed): Tropical Pediatrics. Jaypee Bros: New Delhi, 2002;12,17.
46 Selected Topics in Pediatrics for Practitioners

Breakup Energy Expenditure

How the body utilizes the energy supplied is given below:
Table 4.3
Growth 12%
Physical activity 25%
Basal metabolism 50%
Fecal loss 8%

Table adopted from Pediatric Nutritional requirements. Suraj Gupte (Ed): The Short Textbook
of Pediatrics, 9th millenium edition. Jaypee Bros: New Delhi, 2003.

Daily Requirement for Water

The daily requirements of water at different age groups is given below:
Table 4.4
Age range Water requirement (ml/kg)

First 3 days 80 to 100

3 to 10 days 125 to 150
15 days to 3 months 140 to 160
3 to 12 months 150
1 to 3 years 125
4 to 6 years 100
7 to 9 years 75
10 to 12 years
and thereafter 50

Table adopted from Pediatric Nutritional requirements.The Short Textbook of Pediatrics (9th
edn), Suraj Gupte (Ed), Jaypee Bros: New Delhi, 2003.

Daily Calorie Requirements

Similarly the calorie requirements during the 1st year of life is also very
important.
Table 4.5
Age range (months) Requirement calorie per kg

0 to 3 months 120
3 to 6 months 115
6 to 9 months 110
9 to 12 months 105

Table adopted from Pediatric Nutritional requirements. Suraj Gupte (Ed): The Short Textbook
of Pediatrics, 9th millenium edition. Jaypee Bros: New Delhi, 2003.

Balanced Diets for Children

The following table gives you the balanced diets for children at different
age groups.
 Infant and Young Child Feeding 47

Table 4.6
Preschool Children School Children
1 to 3 years 4 to 6 years 7 to 9 years 10 to 12 years

Veg Nonveg Veg Nonveg Veg Nonveg Veg Nonveg

gm gm gm gm gm gm gm gm

Cereals 150 150 200 200 250 250 320 320

Pulses 50 40 60 50 70 60 70 60
Green leafy 50 50 75 75 75 75 100 100
vegetables
Other vegetables/ 30 30 50 50 50 50 75 75
roots and tubers
Fruits 50 50 50 50 50 50 50 50
Milk 300 200 250 200 250 200 250 200
Fats and oils 20 20 25 25 30 30 35 35
Meat fish – 30 – 30 – 30 – 30
and eggs
Sugar and 30 30 40 40 50 50 50 50
jaggery

Table adopted from Pediatric Nutritional requirements.The Short TextBook of Pediatrics, 9th
millenium edition ed. Suraj Gupte, Jaypee Bros, New Delhi, 2003.

The nutritive value of commonly used food items in different regions

of India is essential for purposes of diet calculation:

NUTRITIVE VALUE OF COMMONLY USED FOODS

Table 4.7
Foodstuff Calories Proteins Foodstuff Calories Proteins
(g) (g)

Cereals Nuts
Wheat 346 11.8 Coconut (dry) 662 6.8
Rice 346 6.5 Cashew nut 596 21.2
Maize 125 4.7 Groundnut 549 26.7
Wheat-flour 348 11.0 Fruits
Pulses Apple 55 0.3
Soyabean 432 43.2 Pineapple 46 0.4
Green gram 348 24.5 Orange 53 0.3
Black gram 347 24.0 Guava 51 0.9
(dal) Tomato (ripe) 20 0.9
Bengal gram 360 17.1 Pomegranate 65 1.6
(whole) Apricot 51 0.6
Bengal gram 372 20.8 Mango (ripe) 53 1.0
(dal) Lemon 57 1.0
Peas 315 19.7 Lichi 61 1.1
(dry) Flesh Foods
Leafy Vegetables Egg 173 13.5
Onion tops 61 4.7 Goat meat 118 21.4
Spinach 26 2.0 Mutton 194 18.5
Mustard leaves 34 4.0 Chicken 300 25

Contd...
48 Selected Topics in Pediatrics for Practitioners

Contd...

Foodstuff Calories Proteins Foodstuff Calories Proteins

(g) (g)

Cabbage 27 1.8 Fish 80-100 18-20

Cauliflower 67 5.9 Milk Products

leaves Cow’s milk 66 3.2
Roots and Tubers Buffalo’s milk 110 4.3
Onion 49 1.4 Human milk 66 1.1
Carrot 48 0.9 Miscellaneous
Potato 97 1.6 Bread 245 7.8
Turnip 29 0.5 Sago 351 0.2
Other Vegetables Sugar 398 0.1
Amla (India 58 0.5 Jaggery 383 0.4
gooseberry) Oil or ghee 900 Nil
Cauliflower 30 2.6
Pumpkin 25 1.4
French beans 48 3.8

Table adopted from Pediatric Nutritional requirements.The Short Textbook of Pediatrics, 9th
millenium edition ed. Suraj Gupte, Jaypee Bros, New Delhi, 2003.

Hence, it is essential that the mother ensures adequate breast feeding,

proper weaning and maintains a balanced diet during the first three
years of growth and development.

BIBLIOGRAPHY
1. Arun Gupta et al. Breast feeding Recent Advances in Pediatrics: Special Vol II
ed Suraj Gupte: Jaypee Brothers: New Delhi, 2002;406,412,433.
2. Shameem Ahamad. Breast feeding Revisited: RAP: Special Vol 3. (Ed) Suraj
Gupte: Tropical Pediatrics. Jaypee Brothers: New Delhi 2002;12,17
3. Suraj Gupte. Pediatric Nutritional Requirements. In Suraj Gupte (Ed): Short
Textbook of Pediatrics (9th millenium edition). Jaypee Brothers: New Delhi,
2002;99,103.
4. WHO/UNICEF. Protecting, Promoting and Supporting Breasfeeding; the Special
Role of Maternity Services, A joint WHO-UNICEF statement, World Health
Organization: Geneva 1989.
 5
Immunization in Practice
A Parthasarathy

Ever since the discovery of Small Pox Vaccine by Edward Jenner,

immunization of children, adolescents and adults have made rapid strides
be it discovery of various vaccines, production technologies or adminis-
tration procedures. Today, we have as many as 25 antigens at the Global
Scenario and about 15 antigens in India. So much so we have to categorize
the available antigens, viz.
1. Infant immunization (universal vaccines) BCG, DPT, OPV, Measles, HB,
Hib
2. Toddler immunization (additional vaccines/booster) Under 5 years: MMR,
DPT, OPV and Hib Booster, Typhoid, Varicella, Hep A Vaccines, Hep
A and Hep B (catch up)
3. Adolescent immunization TT/Td Booster, MMR, R, Typhoid, Hep A,
Varicella, Hep A and Hep B? (catch up)
4. Adult immunization HB, Typhoid, TT Booster, Hep A, Varicella, Hep
A and Hep B (?catch up)
Certain emerging trends in pediatric and older children immunization
are fascinating:
1. Changes in immunization schedules based on current scientific
evidences of primary doses and long-term follow-up and minimum
interval between primary vaccine doses.
2. Use of monovalent and combination vaccine formulations.
3. DPT used as a solvent to dissolve Hib.
4. DPT-HB used as a solvent to dissolve Hib.
5. Interchangeability of vaccine formulations
6. Use of thiomersal as the preservative.
7. Use of auto destruct syringes.
8. Post polio eradication policy, NID’s and AFP surveillance.
9. Campaign for intensified routine immunization coverage.
10. Introduction of more childhood vaccines in the universal
immunization program.

Changes in Immunization Schedules

Though, the World Health Organization has developed an Universal
Schedule for EPI vaccines, each country has to formulate its own National
Immunization Schedule based on the following 5 criteria:
50 Selected Topics in Pediatrics for Practitioners

1. Epidemiological relevance
2. Immunological appropriateness
3. Technical feasibility
4. Economical viability and
5. Socio cultural acceptability.
Thus in India today we have the standard 6 antigens as Scheduled
Vaccines viz., BCG, OPV, DPT and Measles in the National Immunization
Schedule and the 7th antigen viz. HB has since been included in the
pilot project areas based on epidemiological relevance. To introduce
MMR and Typhoid vaccines in the National Schedule it might take some
more time. All the vaccine formulations currently being used in India,
monovalent/combination vaccine formulations have since been licensed
by the Drugs Controller General of India based on Immunological
appropriateness. The technical feasibility of manufacturing BCG, DPT,
DT, TT and HB in India, have since picked up momentum resulting in
low cost indigenous vaccines. In view of the low cost indigenous vaccines
and subsidy from International organizations and Global Alliance for
Vaccines and Immunization the economical viability has come to stay
and the socio cultural acceptability has resulted in marked decline in the
6 vaccine preventable diseases wherever the coverage has been near
100 per cent.
With increasing number of OPV doses during PPI campaign, the
number of primary doses remain as 4 doses only viz., Birth, 6, 10, 14
weeks followed by repeat doses at 16 to 18 months and 5 years. The
country has been divided into high, intermediate and low prevalence
poliomyelitis zones resulting in different strategies for PPI doses. 3 doses
of the HB vaccine given during infancy even with a minimum interval
of 4 weeks is found to elicit anamnestic response during long term
follow up thus resulting in no booster doses.

Use of Monovalent and Combination Vaccine Formulations

The use of combination vaccine formulations is not new. DPT, OPV,
MMR, DPT, IPV Combination formulations are in wide use for long
years. DPwT-HB, DPacT-HB, DPacT-HB-IPV, DPac-HB-IPV-Hib, HepA-
HepB are some of the newer Combination formulations now licensed
and in use in over 150 countries of the World. WHO also recommends
the use of these vaccines appropriate to the schedule being practiced in
a particular nation coinciding with the number of primary/booster doses
recommended. For instance in India, DPwT—HB vaccine is very much
compatible for the 2nd and 3rd doses after the administration of
monovalent HB vaccine at birth. Similarly at 6,10,14 weeks combined
DPT-HB, Hib vaccine formulation can be given using DPT-HB as a
diluent or DPT + Hib for extraneous mixing.
 Immunization in Practice 51

DPT used as a Solvent for Hib and DPT-HB as a Solvent for Hib
DPT now has been found to be compatible when used as solvent for Hib
vaccine, which is supplied as a lyophilized pellet. So also, DPT-HB can
be used as a solvent to dissolve Hib vaccine. But caution should be
exercised to study the manufacturer’s recommendations. Only the
recommended formulations can be combined with each other and the
scientific evidence for the same viz., WHO certification or a published
article in an Indexed Journal etc. should be looked into carefully. The
efficacy of combination vaccine formulation have since been established
beyond doubt and combination vaccines have become the order of the
day in many developing countries because of low cost, increased
compliance, decreased clinic visits, high immunogenicity and reduced
adverse effects.

Interchangeability of Vaccine Formulations

Where multiple doses of the same vaccine are needed for purpose of
primary immunization starting the vaccine with a particular formulation
for the first dose and using a different formulation for the 2nd and 3rd
doses are found to be comparable now without compromising on
immunogenicity. However this situation should be reserved only when
a particular formulation indicated earlier is not readily available, other-
wise ideal will be to continue with the same formulation.

Use of Thiomersal as the Preservative

WHO, has since shelved the controversy on the use of THIOMERSAL
as the preservative. Being, an ethyl mercury, it does not produce any
neurotoxicity unlike methyl mercury. With 25 mcg for each vaccine
administration the cumulative effect on neurotoxicity, once feared is no
more a concern. However for methyl mercury maximum daily limits
have to be set for fear of neurotoxicity. Hence, there is no need for
Thiomersal free vaccine formulations used in EPI antigens.

Use of ‘Auto Destruct Syringes’

Injection safety concerns have resulted in the development of ‘Auto
Destruct Syringes’. In this new syringe device the plunger gets self-
locked after a single use, thus preventing the use of the disposable
syringe any more. Currently, these types of syringes are being used in
pilot projects for HB vaccine, with GAVI funding. GOI-Government of
India will introduce ‘Auto Destruct Syringes’ in routine immunization
program in due course of time. They are not very expensive and universal
usage will bring down their cost further.
52 Selected Topics in Pediatrics for Practitioners

Post Polio Eradication Policy, NID’s and AFP Surveillance

IPV vs OPV
WHO in its recent Global Advisory Committee meeting in France, has
debated the combined use of OPV and IPV in developing countries as
a post eradication policy as being practised in some developed (Polio
Eradicated) countries now, for fear of Vaccine Associated Paralytic
Poliomyelitis (VAPP) viz., one dose of IPV followed by 2 or 3 doses of
OPV. However this schedule is not fool proof. The merits and demerits
of OPV vs IPV need to be considered carefully:

Oral live attenuated Polio Vaccine (OPV) and Injectable

Enhanced Inactivated Polio Vaccine (IPV)–Comparison

Characteristics OPV IPV

• Prevents Polio Yes Yes

• Humoral Immunity Yes Yes
• Intestinal Immunity Yes Some
• Duration of Immunity Long Long
• Contact Immunization Yes No
• Virus excretion Yes No
• VAPP Rare No

The Asian Experts Bureau on Vaccines Consensus Statement 1999

Observes.
1. OPV is the basic vaccine for countries that still have wild poliovirus
circulating in the community.
2. IPV provides immunity to the individual vaccinee and in some situa-
tions gives better seroconversion than OPV.
3. The principal safety problem with polio vaccine is VAPP after OPV,
which is perceived differently in different countries.
4. Many countries in the Asian region have concerns about importation
of Wild Polio Virus.
5. Every country has a permissive policy with regard to the use of IPV
in private patients. Moreover, cost aside, every country indicated
that IPV combination would eventually be adopted.
6. It is likely that the schedule will first be sequential IPV/OPV.
7. Every country recommends IPV for Immunocompromised patients.
Logisticswise, from the point of view of IPV production as against
the manufacturing capacity of 1-2 Billion doses per annum for OPV, that
for IPV is less than 100 million doses, as it is used more or exclusively
in western countries. As at present United States of America, Canada,
 Immunization in Practice 53

France, Germany, the Netherlands, Finland, Norway and Sweden (some

of polio-free western countries with low risks of importation of wild
virus) have already been using the strategy of full IPV regimen.

National Immunization Days (NID’s) PPI

As for as NIDs are concerned, in North East region of the Country
where Polio is still endemic 3 NID’s and 2 sub NID’s with door to door
coverage will be the strategy. In other parts of the Country only 2 NID’s
will be adopted. From 2003, the NID’s are being conducted in January
and February of each year with mop up by door-to-door coverage.

AFP Surveillance
More emphasis will be made on stool collection, follow up and virological
confirmation through active laboratory surveillance. Integrated Disease
Surveillance System will be developed to incorporate other VPD
surveillance also in due course of time.

Campaign for Intensified Routine Immunization Coverage

Wherever the routine immunization coverage is poor, efforts will be
made through door-to-door intensified campaigns to achieve a near
100% coverage for UIP vaccines. The help of number of professional
bodies like IMA, IAP, FOGSI etc will be sought to achieve the target.

Introduction of More Childhood Vaccines in

the Universal Immunization Program
An Advisory Committee on Immunization Practices in India (ACIPI),
has since been formed, with representatives of GOI, ICMR, IMA, IAP,
FOGSI, Microbiologists, Community Medicine Experts and individual
experts as members. This committee will recommend introduction of
additional vaccines that are currently licensed in India in the UIP in a
phased manner. As a first step, HB vaccine is being introduced at 6,10,14
weeks in the DPT schedule in certain pilot project areas where the
routine immunization coverage in above 95 percent. MMR, Typhoid
vaccines may be the next vaccines of choice.
In the mean time, the Indian Academy of Pediatrics has come out
with a practical and epidemiologically relevant Immunization Time Table
for its members.
54 Selected Topics in Pediatrics for Practitioners

IAP IMMUNIZATION TIME TABLE

Age recommended
Vaccine Primary Booster

BCG Birth—2 weeks No booster

OPV Birth, 6, 10, 14 weeks 16-18 months, 5 years
DPT 6,10,14 weeks 16-18 months, 5 years
Hepatitis B Birth, 6, 14 weeks No Booster
Hib Conjugate 6, 10, 14 weeks 16-18 months
Measles 9 months plus No Booster
MMR 12 months No Booster
Typhoid WC 6 months 2 doses Once in 3 years
(or) Vi 2 years 1 dose Once in 3 years
(or) Ty21a 6 years 3 doses Once in 3 years
TT / Td 10, 16 years Once in 5 years
TT (Pregnant Women) 2 doses Once in 5 years

ADDITIONAL VACCINES

Varicella** Above 1 year and No Booster

< 12 years 1 dose
> 12 years 2 doses
Hepatitis A** Above 2 years 6 months later
1 dose on elected date

Note
1. Newborns who miss BCG, OPV and Hepatitis B vaccines at birth
should receive the same latest at the completion of 6 weeks.
2. Hepatitis B/Hib vaccines can be given in combination formulation.
3. In addition to ‘Routine OPV doses’ the recommended ‘Pulse OPV
doses’ are also mandatory during PPI campaigns.
4. Apart from the earliest age indicated, MMR, Typhoid, Varicella and
Hepatitis A vaccines can be given for older children, adolescents and
adults.
5. Td (Tetanus/diphtheria toxoid) should be preferred to TT (Tetanus
toxoid where available).
6. Varicella** and Hepatitis A** are additional vaccines as recommended
by Indian Academy of Pediatrics.

ADOLESCENT IMMUNIZATION
In India, adolescent immunization is presently gaining momentum.
Though the national immunization schedule provides only tetanus toxoid
as the only vaccine for the adolescents, the need for other vaccines
 Immunization in Practice 55

during the adolescent period are being stressed by the professional

bodies like Indian Academy of Pediatrics. Recommendations from the
Academy have been forwarded to the Government of India for inclusion
of MMR, rubella, typhoid vaccines, etc. It is fervently hoped that more
vaccines will find a place soon in the National Immunization Schedule
other than Tetanus toxoid.

IAP ADOLESCENT IMMUNIZATION TIME TABLE

Vaccine Age Recommended

Tetanus Toxoid Booster doses at 10 and 16 years. Booster every 5 years

Rubella Vaccine (As part of For girls at 12-13 years of age, one dose, if not given earlier.
MMR vaccine or Monovalent
formulation)
MMR Vaccine* Both for Boys and Girls one dose at 12-13 years of age,
if not given earlier.

Hepatitis B Vaccine# 3 doses, any age at 0, 1 and 6 months, if not given earlier.
(0 being elected date)
Typhoid Vaccine Every 3 years
TA (Whole cell),
Vi or Oral Ty21a
Varicella Vaccine 10-12 years one dose, > 13 years two doses at 4 weeks interval

Hepatitis A Vaccine# 2 doses at 0 and 6 months (0 being elected date)

* 2 doses of MMR vaccine are recommended for those travelling to USA.

# Combined Hep A + Hep B vaccine adult formulation can be given at 0, 1 and 6 months (0
being elected date)

General Rules of Immunization—Ten Commandments

1. Keep all vaccines at +2 to +8oC. Do not freeze DPT, DT, TT, HB,
Hib, and HA + HB aluminium salt adjuvanted vaccines. If VVM
is used do not use OPV when the colour of the square and circle
match with each other. For such vaccine requiring multiple doses,
e.g. DPT, DT, TT, HB, Hib, MMR, OPV, Typhoid (WC), Varicella
above 13 years, maintain minimum 4 weeks interval between the
recommended doses.
2. Two viral vaccines like MMR, Varicella can be given together; but
if given separately 4 weeks interval should be maintained.
3. DPwcT can be used as solvent to dissolve the pellet of Hib vaccine.
4. DPwcT/HB vaccine can also be used as a solvent to dissolve the
pellet of Hib vaccine.
5. When extemporal mixing is done as described above make sure
that the antigen of the same manufacturer must be used and should
insist on WHO/DCGOI certification.
56 Selected Topics in Pediatrics for Practitioners

6. For low birth weight and pre-term babies a rule of two approach
may be adopted. Viz. baby must be two months old, and weigh
two kgs. Irrespective of the period of gestation/birth weight, all
vaccines can thus be given as per schedule of normal baby.
7. Position the child properly according to oral or injectable vaccine.
8. Clean the site of immunization with an antiseptic from medial to
lateral aspect.
9. Always use autodestruct syringes where available.
10. Do not rub the site of inoculation vigorously. Gentle pressure for
a few seconds is sufficient.

Trends in Immunization will Keep Changing as

More Newer Vaccines are Made Available
Newer Vaccines: Vaccines Newly Licensed in India
The term newer vaccines is a misnomer in the Indian context. Most of the
vaccines recently licensed in India are almost already one or two decades
old and a few about 5 to 6 years old. It will be appropriate to call them
newly available or newly licensed vaccines in India. For all practical
purposes those vaccines, which are not included in the National Immuni-
zation Schedule for routine use and certain other vaccines considered as
additional vaccines on epidemiological prevalence or under special
circumstances will come under the purview of newly licensed vaccines.
For purpose of this resume the following vaccines will be discussed
in detail.
1. Hepatitis B vaccine
2. Hib vaccine
3. MMR vaccine
4. Typhoid vaccine
5. Varicella vaccine
6. Hepatitis A vaccine
7. Pneumococcal vaccine
8. Influenza vaccine
9. Meningococcal vaccine
10. Combination vaccines
a. DPwcT-HB vaccine
b. DPwcT-Hib conjugate vaccine
c. DPwcT-HB / Hib conjugate vaccine
d. Hep A-Hep B vaccine

Characteristics of Newly Available Vaccines

Hepatitis B Vaccine
Sterile suspension contains purified major surface antigen of the
recombinant DNA preparation adsorbed on to aluminium hydroxide.
 Immunization in Practice 57

The pediatric formulation contains 10 μgm and is recommended at

birth, 6 and 14 weeks for universal infant immunization. For older
children above 1 year and upto 10 years the pediatric formulation is
recommended at 0, 1 and 6 months schedule. The adult formulation of
20 μgm (in 1.0 ml suspension) recommended at 0,1,6 months schedule
should be administered IM in deltoid region. More than 10 monovalent
vaccine formulations are now available in India. All yeast derived DNA
recombinant vaccine formulations licensed in India are equally immuno-
genic. Hence, interchangeability between doses is also permissable. No
booster dose is needed. Thiomersol (ethyl Mercury) is used as a
preservative.

Hemophilus Influenzae Type b Conjugate Vaccine

A lyophilized formulation of purified polyribosyl-ribitol-phosphate
capsular polysaccharide (PRP) of Hib, covalently bound to tetanus
toxoid/diphtheria toxin CRM197. Lactose is the stabiliser. Each single
dose of vaccine contains 10 μgm of purified capsular polysaccharide
covalently bound to 20–40 mgm of tetanus toxoid/diphtheria toxin
CRM197, AlOH adjuvanted. Hib immunization is age dependent and
is confined to children less than 5 years only.
Doses

Age Primary Booster

0-6 months 3 doses 15-18 months

6-11 months 2 doses 15-18 months
12-14 months 1 dose 15-18 months
15-59 months 1 dose No booster

For infants who have already suffered from Hib meningitis or other
Hib invasive diseases.
a. If child is less than 2 years—immunize with a single dose 1 month
after recovery.
b. If child is more than 2 years—no need for Immunization

MMR Vaccine
The three live attenuated viruses, as a single dose of vaccine in a lyophi-
lised form contains at least 1000 CCID50 of the Measles virus strain
edmanston Zagreb, produced from human deploid cells, at least 5000
CCID50 of live attenuated Mumps virus strain(Zagreb produced from
chick embryo cells and at least CCID 100050 of live attenuated rubella
strain plotkins RA27/3 cultural in human deploid cells (strains available
in India). Single dose of 0.5 ml to be administered subcutaneously. True
58 Selected Topics in Pediatrics for Practitioners

allergy to eggs proteins (anaphylactic reaction after ingestion of eggs)

and recent injection of immunoglobulin and pregnancy are
contraindications. For routine infant immunization a single dose is
recommended at 12-15 months. For adolescents beyond 10 years and for
adults also only one dose is recommended in our country. However,
travelers to USA will be required to take 2 doses at 4-6 weeks interval.

Typhoid Vaccine
The pediatric formulation of whole cell typhoid vaccine can be given
from 6 months onwards in 2 doses of 0.5 ml at 6-8 weeks interval for
children beyond 2 years the Vi CPS antigen is recommended. Both Vi
CPS polysaccharide vaccine and Oral typhoid vaccine containing 25mcg
of purified Vi CPS antigen extracted from Ty21a strain offer a protection
from 7-15 days after vaccine administration and lasting immunity for 3
years are available for adolescent immunization. Vi CPS antigen is to be
given as a single dose IM and Oral Ty21a vaccine as 3 doses on days
1, 3 and 5 irrespective of age above 6 years. The capsule should be
swallowed before food. S.typhi sensitive antimicrobials like Co-
trimoxazole, Chloromphenicol, Ciprofloxacin, etc. should be withheld at
least one week prior to and after administration of the Oral typhoid
vaccine.

Varicella Vaccine
The lyophilised OKA strain of Chicken Pox (Varicella) vaccine is available
as a pellet to be reconstituted with a solvent. Preferably given in deltoid
by subcutaneous route in 0.5 ml dose. A single dose is recommended for
children below 12 yrs starting from > 1 year. Two doses are recommended
at 4-6 weeks interval for children > 13 years. Shake test must be done
for the presence of any foreign particle before vaccine administration.
Absolute contraindications include an attack of natural infection prior
to vaccination, pregnancy and an absolute lymphocyte count less than
1200 per mm3 or presenting other evidence of lack of cellular immune
competence. The Varicella vaccine if preferred for childhood
immunization can be given from 1 year onwards. A single dose is
recommended with no booster.

Hepatitis A Vaccine
Hepatitis A virus vaccine is a sterile suspension containing formaldehyde
inactivated Hepatitis A virus (HM 175 Hepatitis A strain) adsorbed into
Aluminium hydroxide should be administrated by IM route in deltoid
muscle. In patients with thrombocytopenia or bleeding disorders the
vaccine should be administered subcutaneously. A single dose of 0.5 ml
 Immunization in Practice 59

containing 720 ELISA units is indicated from 2 years upto 18 years, both
for children and adolescents. Single dose of adult formulation contain
not less than 1440 ELISA units of viral antigen in 1 ml suspension and
indicated in adolescents above 19 years and in adults.

Pneumococcal Polysaccharide Vaccine

7-valent conjugate pneumococal vaccine suitable for routine infant
immunization at 2, 4, 6 months is now available abroad. This preparation
covers the commonly prevalent serotypes of pneumococci responsible
for 85% of pneumococcal infections. To be given by IM route 0.5 ml
dose. Booster: 1 dose is given after 3-5 years. Indications under special
circumstances include.
1. Sickle cell disease
2. Functional or anatomic asplenia
3. Nephrotic syndrome and chronic renal failure
4. Conditions associated with immunosuppression such as organ or
bone marrow transplantation, drug therapy or cytoreduction
therapy (including long-term systemic coticosteroid therapy).
5. HIV infections
6. CSF leaks
7. CCF or cardiomyopathy
8. Cystic fibrosis
9. Diabetes
10. Cirrohosis of liver

Influenza Vaccine
Inactivated purified split influenza vaccine contains 2A+ 1B type antigens.
(WHO determines composition of antigen on seasonal basis mostly in
US, European countries, Australia etc) 0.5 ml of vaccine contains 15 mg
haemagglutinin of each of recommended strains phosphate buffered
saline, saccharide, thiomersol and traces of formaldehyde (used for
inactivation). In countries which practice routine Influenza Immunization
one dose of 0.5 ml for children over 6 years of age and adults and 2
doses of 0.25 ml for children 1 to 6 years at interval 4 to 6 weeks. High
risk groups indications include:
1. Asthma and other chronic pulmonary disease, e.g. cystic fibrosis
2. Hemodynamically severe cardiac disease
3. Immunosuppressive disorder or therapy
4. HIV infections
5. Sickle cell anemia and other hemoglobinopathies
6. Diseases requiring longterm aspirin therapy
7. Chronic renal dysfunction
8. Chronic metabolic diseases including diabetes mellitus, etc.
60 Selected Topics in Pediatrics for Practitioners

Meningococcal A + C Vaccine
Lyophilised preparation of purified polysaccharides from Neisseria
meningitidis sero groups A and C. 0.5 ml reconstituted vaccine formu-
lation contains 50 mcg of polysaccharide A and C with sterile saline
solution as diluent and phenol as preservative in multidose presentation.
Protection offered against A and C sero groups of N meningitidis
indications:
1. Children from 2 years of age and adults in endemic areas
2. Visitors to endemic or epidemic areas
3. Subjects living in closed communities and close contacts of infected
patients. Single dose 0.5 ml of vaccine is given subcutaneously by
completely dissolving the diluent to the vaccine pellet. To be stored
at +2 to +8°C.

Combination Vaccines
Combination vaccines have become the choice of the day in developed
countries. It is time for countries like India to consider the currently
available combination vaccines. Though it may take time to introduce
combination vaccines in the National Immunization Programme, IAP
advocates its members to consider the use of combination vaccines.
DPT-HB, DPT-Hib, Hep A-Hep B are currently available combination
vaccines in our country. Intelligent scheduling of these vaccines in tune
with the National Immunization Schedule has been suggested by IAP.
DPT is used as a solvent to dissolve the pellets of Hib conjugate
formulation and DPT-HB is used to dissolve the pellets of Hib conjugate
vaccine. DPT-HB / Hib, a Pentavalent formulation is ideal for India. US,
Canada, France etc. are already using DPacT-IPV-HB-Hib as Hexavalent
combination vaccine.

DPwcT-HB Vaccine
Fluid formulation. 0.5 ml pediatric dose contains not less than 30 IU of
adsorbed D-Toxoid, not less than 60 IU of T-Toxoid, not less than 4 IU
Pw and 10 mgm of recombinant HBsAg protein. To be stored in +2 to
+ 8°C. Not to be frozen because of aluminium adjuvantation. To be
administered deep IM in anterolateral thigh. Can be given at 6, 10, 14
weeks schedule, for babies born to HBs Ag-Ve mothers.

DPwcT-Hib Vaccine
Fluid formulation of 0.5 ml of pediatric dose contains DPT vaccine with
D-Toxoid, Pw and T-Toxoid as described above with lyophilized pellet
of 10 mgm of purified capsular polysaccharide covalently bound to 20
 Immunization in Practice 61

to 40 μgm of tetanus toxoid. DPT is used as a solvent to dissolve the

pellet of Hib conjugate vaccine.

DPwcT-HB / Hib Vaccine

0.5 ml of DPwcT-HB vaccine formulation can be used as a solvent to
reconstitute the lyophilized pellet of Hib conjugate vaccine to make it
a pentavalent formulation which can be administered at the anterolateral
thigh at 6, 10, 14 weeks. Shake test must be done before administration
for any visible particles. To be stored in +2°C to +8°C.

Hep A-Hep B Vaccine

Combination formulation of Hep A + Hep B antigens. Aluminium
adjuvanted with thiomersal as preservative. Two different formulations
are available.
Pediatric formulation 0.5 ml—contains 360 ELISA units of Hep A and 10
mgm of recombinant HBsAg protein antigen. Schedule: 0, 1, 6 months.
Site and route of administration: Anterolateral thigh, deep IM. The vaccine
should be stored in +2 to +8°C. Not to be frozen.
Adult formulation 1.0 ml—contains 720 ELISA units of Hep A and 20
mgm of recombinant HBsAg protein antigen. Schedule: 0, 1, 6 months.
Site and route of administration: deltoid region, deep IM. The vaccine
should be stored in +2°C to +8°C. Not to be frozen.
As more and more vaccines are discovered the schedule will perhaps
contain more of combination formulations in the future. Affordable
indigenous combination formulations will be a great boon to Indian
children and this will become a reality in the near future.

BIBLIOGRAPHY
1. Parthasarathy A, Dutta A K, Swati Bhave. IAP Guide Book on Immunization
2001. Know your vaccines: Publication of Indian Academy of Pediatrics: Mumbai
2001; and updated in June 2002;61-70.
2. Parthasarathy A, Dutta A K, Swati Bhave. IAP Guide Book on Immunization
2001. IAP Policies, Guidelines and Recommendations: Publication of Indian
Academy of Pediatrics: Mumbai, June 2001 and updated in June 2002;72-77.
 6
Approach to the Diagnosis and
Management of a Febrile Child
S Thangavelu

Fever is a common symptom which prompts the parents to bring their

children to the Pediatrician. Though fever is considered to be a protective
phenomenon it may turnout alarming to the parent when the child
manifests with fever associated seizures. From the common viral fever
to fever associated with many bacterial infections and the fever with
loss of conciousness signalling a meningeal involvement or to the fever
of unknown origin (FUO), the practitioner has to develop a systematic
approach to the diagnosis and management of a febrile child.
This approach will be discussed under the following headings:
• Definition
• Ideal site/thermometer
• Physiology
• Clinical approach
• Categories
• Short-term fever
• Tips for examination
• Fever with focus
• Fever without focus
• Prolonged fever
• PUO
• Recurrent fever
• High-risk child
• Management of fever
• Antipyretics
• Physical measures
• Parental education.
About 20 percent of the emergency visits of a sick child is for fever.
About 10 percent of all hospital admissions is for fever evaluation. Fever
is a symptom, the underlying disease may be a self-limiting problem
like viral fever or an invasive bacterial disease requiring aggressive
treatment like meningitis. A pediatrician’s role is to strike a balance
 Approach to the Diagnosis and Management of a Febrile Child 63

between overtreating a viral fever or failing to identify and treat a

serious illness like meningitis.

Definition and Basic Facts

Fever is a controlled increase in body temperature above the normal
values for an individual. Children are generally considered as febrile
when their rectal temperature is greater than 38.0o C (100.4o F).
or
A oral temperature above 37.5o C (99.7o F)
or
An axillary temperature above 37.0o c (99.0o F).

What is the Ideal Site? Ideal Thermometer?

An ideal site should be close to the major arteries, should not have local
inflammation and must be safe and should not be influenced by external
temperature or processes like drinking water.
Rectal temperature measurement is the most ideal, regards to precision
and not influenced by extraneous factors. But considering the risk of
rectal perforation, though remote, emotional trauma and chances for
spreading infection, it is not widely practiced. But still it is ideal in
young infants and toddlers.
Oral or sublingual measurement is useful in co-operative older
children who do not have increased respiratory rate, have not taken
food or liquid in the previous hour.
Axillary measurement may lack precision but practiced for conve-
nience. Tympanic membrane has been recently used with great accuracy
and reproducibility beyond 6 months of age. They are operator dependant
and need correct positioning. It is expensive and not freely available in
our country.

Ideal Thermometer
Glass thermometers are still the gold standard. But long dwelling time
and potential breakage are disadvantages.
Liquid crystal forehead strips are inconsistent.

How Temperature is Regulated?

Hypothalamus dictates the temperature in which body has to maintain
by adjustment of thermostat.
It is carried out by regulating effector mechanisms in the following
way. In a normal individual it is fixed at 37o C and when child develops
infection, endogenous pyrogens stimulate the hypothalamus to reset the
thermostat to the higher temperature—say at 39o C.
64 Selected Topics in Pediatrics for Practitioners

Effector mechanism for Effector mechanism for

Heat loss 37o C Heat Production 39o C

Infection 39o C

Antipyretics
Response to fever

To decrease body temperature To increase body temperature

Behavioural Behavioural
Sunbath posture Curling up
Removing the clothes Putting on more clothes
Baby cries for attention Baby cries for attention
Physiological Physiological
Cutaneous vasodilation Cutaneous vasoconstriction
Sweating Thermogenesis
Shivering and
Non-shivering

GENESIS OF FEVER
Exogenous Pyrogen

Endogenous Pyrogens
(IL-1, IL–6, TNF α, INTFR)

Reset the set point in Thermostat in

Hypothalamus say (from 37 to 39o C)

Hypothalamus considers this (37o C) as

subnormal when compared to set point (39o C)

Heat Synthesis
Effector mechanisms for heat production
(Behavioral and physiological)

Fever develops

Clinical Approach
Clinical spectrum of a febrile child is wide and complex.
1. Benign self limiting viral infections, which may not need investigations
and safely treated with only antipyretics, frequent examinations and
reassurance.
 Approach to the Diagnosis and Management of a Febrile Child 65

2. Children with simple bacterial infections like tonsillitis or skin and

soft tissue infection may require simple investigations like throat
swab and CBC. They fully recover with oral antibiotics like
amoxicillin, penicillin, erythromycin or cephalexin.
3. Serious infection like meningitis—warrant frequent examination and
suspicion. Once the diagnosis is suspected they need hospitalization,
invasive investigation like lumbar puncture and parenteral antibiotics
for 10-14 days. Prior administration of powerful oral antibiotics can
modify the picture, failure to make the diagnosis and may lead to
under treatment and complications.
So management decisions are based on following factors:
I. Duration of illness
II. Presence or absence of toxemia or sick look
III. Presence or absence of focus of infection
IV. Risk factors in host
V. Lab criteria—low or high risk. Presence or absence of leucocytes,
neutrophillia or raised CRP
VI. Age of the host.
Hence a febrile child is categorized into following groups based on
duration and risk factors.
1. Short-term fever (less than one week)
2. Prolonged fever with localizing signs (more than one week with
some localizing signs)
3. Pyrexia of unknown origin
4. Recurrent fever
5. Fever in a high-risk host , irrespective of duration.
Though this may appear to be an oversimplified one, it will be
practically useful to take decision regarding investigation and
management.

Short-term Fever

This forms the major group among outpatients. Following illnesses

present with short term fever.

Short-term Fever

With focus Without focus

1. Problematic viral infection 1. Benign viral infection
2. Bacterial infection with focus 2. Occult bacteremia without focus
3. Malaria
66 Selected Topics in Pediatrics for Practitioners

1. Benign viral infections Benign viral fevers are caused by rhino, para
influenza, adenoviruses and respiratory syncytial viral infections.
Usually they present with URI symptoms like rhinorrhea, cough,
throat pain in addition to fever, anorexia, headache and body pain.
They will show diffuse involvement of upper respiratory tract with
suffused conjunctiva. Apart from these symptoms there may not be
any focus of infection. They may have seasonal pattern and frequently
affect other family members within a short period. Diagnosis is usually
made clinically by exclusion and uneventful recovery following a
short febrile illness.
2. Problematic viral infections Viral exanthemas such as measles, German
measles and chicken pox are to be suspected in an unimmunised
child with history of exposure to a patient with illness. Dengue fever
is another epidemic viral infection to be considered in the potential
season.
3. Other serious viral infections are acute viral hepatitis, viral encephalitis
and viral myocarditis.
4. Malaria is one of the common short-term fever seen in an endemic
area when the child has fever with rigor, pallor and splenomegaly.
5. Bacterial infection with (focus) localizing signs Common causes are
pharyngitis, urinary tract infection, skin and soft tissue infection,
bone and joint infection, and acute CNS infection. During every visit,
pediatrician should ask for localizing symptoms and look for localising
signs, because fever is a dynamic problem and the child may improve
or worsen even within hours.
6. Occult bacteremia without (focus) localizing signs Usually bacteremia is
associated with definite focus of infections such as pneumonia,
meningitis or osteomyelitis. In 6 percent of children with fever below
36 months of age there is bacteremia without focus. Occult bacteremia
without focus will be easily mistaken for viral infection because of
absence of focus. It needs to be differentiated because the former
needs antibiotics and later does not need as it is self limiting.

TIPS for Physical Examination

Careful and skilled observation is the key to diagnosis, which is based
on the ability of physician in distinguishing toxic from nontoxic children.
We should also remember the fact that febrile illness is a dynamic
one, because a well looking child in the morning may worsen in the
evening, stressing the need for repeat physical examination. Examining
in the following sequence will help for completing the examination.
 Approach to the Diagnosis and Management of a Febrile Child 67

1. Observe from distance, without touching the child

Count respiratory rate, look for respiratory distress and eye contact
to assess consciousness. Once the child cries, these signs could not
be elicited.
2. Keeping in mother’s lap, signs requiring child’s co-operation to be
elcited next
• Wave a torch light and see whether he follows
• AF, neck stiffness
• Hydration, icterus
• Spleen or liver
• Extremities—skin for pallor, rash or for cold extremities
• Perfusion—pulse, CRT
3. Little invasive
• Throat exmination
• Looking for phimosis
4. If sleepy, wake up and assess the level of consciousness
• If irritable and crying, reexamine the child when he is quiet or the
examiner should stay out of the child’s view and continue the
examination.

Symptoms/signs Possible Diagnosis Investigation

• Respiratory symptoms Viral URI None

no focal signs
• Inflamed tonsils Tonsillitis Throat Swab, CBC
• Cough, chest pain, Bronchiolitis, Asthma, CBC, X-ray
dyspnea Pheumonia, Empyema
• Ear pain, inflammed Acute otitis media Consult ENT Surgeon
tympanic membrane
• Skin rash Viral Exanthem,
drug allergy, dengue
• Purpura Dengue, leukemia, CBC, Dengue serology, Urine culture,
septicemia, aplastic blood culture smear, X-ray chest
anemia, meningococcal
septicemia
• Abdominal pain Dengue, appendicitis, CBC, Dengue serology, Urine culture,
colitis, viral hepatitis, SGPT,Bilirubin, widal, surgical
UTI,Enteric fever consultation, USG Abdomen
• Icterus Viral Hepatitis, Malaria SGPT, Bilirubin, smear for MP, QBC
Leptospirosis Viral study, MAST
• Disproportionate Myocarditis, rheumatic ECG, X-ray chest, ECHO ASO, CRP, ESR
tachycardia fever
• Joint, limb swelling Arthritis, osteomyelitis, Orthopedic opinion, X-ray CBC,
Rheumatic fever, ESR, CRP, ASO
leukemia

Contd...
68 Selected Topics in Pediatrics for Practitioners

Contd...

Symptoms/signs Possible Diagnosis Investigation

• Lymph node Regional lymphadenitis, CBC, Mx, CXR smear study

enlargement leukemia, filariasis
rubella, tuberculosis,
infectious mononucleosis
• Convulsion, altered Febrile convulsions CSF analysis, CT scan, EEG
level of consciousness Meningitis, encephalitis Dengue serology CBC, USG abdomen,
• Heptomegaly Dengue, hepatitis, liver LFT, ECG, ECHO, CXR
abscess, myocarditis with
failure
• Splenomegaly Malaria, enteric fever, Smear study QBC, widal
leukemia
• Pallor Malaria, leukemia, CBC, smear study MP, QBC
aplastic anemia
• Shock Septic shock, dengue, Blood culture, evaluation for dengue and
myocarditis with myocarditis
cardiogenic shock

Management option in a febrile child with focus is decided by the

severity of infection.

Fever without focus—Management

Main aim of the clinical approach to a febrile child is to identify the
cause of fever without focus, whether it is occult bacteremia or viral
infection. Management options available for a febrile child < 36 months
without focus are
a. Only antipyretics
b. Antipyretics + antibiotics (oral or parenteral)
c. ++ investigations
d. +++ hospitalization
Option is decided by following factors
a. Age of the child
b. Presence or absence of toxic look
c. Height of the temperature
d. Laboratory criteria—Low risk or high risk
Low-risk Lab test High-risk

5000-15,000/mm3 Total count > 15,000/mm3

< 5000/mm3 Absolute neutrophill count > 10,000/mm3
Negative CRP Positive
Pus cells absent Urine analysis Pus cells present

In all febrile children less than 36 months old with toxic appearance,
plan hospitalization,investigation and antibiotics.
 Approach to the Diagnosis and Management of a Febrile Child 69

In all febrile children less than 36 months without toxic appearance

management decision is made by age of the child, height of temperature
and the laboratory criteria.
1. In Infants < 3 months Serious bacterial infection is present in 10-15
percent of infants less than 3 months, who usually have a rectal
temperature of 39° C or greater. Clinical judgment in these young
infants is often difficult and incorrect. Physical examination may fail
to reveal specific findings despite the presence of systemic infection.
Hence they need early investigations and hospitalization unless they
have low risk laboratory criteria. Elicit the history, detail physical
examination and do basic investigations like CBC, urine analysis. If
total WBC count is between 5,000 to 15,000/cmm, absolute band
count < 1500/cmm, urine analysis is normal and CRP is negative,
serious bacterial infection is less likely. On the contrary abnormal
laboratory tests warrants hospitalization.
2. Infants aged 3 months to 3 years Approximately 30 percent of febrile
children in this age group have no localizing signs of infection. Occult
bacteremia is observed in 4 percent of relatively well appearing febrile
children without focus. This is due to S.pneumoniae, H.influenzae,
N.meningitis or salmonella. If temperature is < 39° C follow up as
outpatient with only antipyretics without investigation or antibiotic. If
temperature is > 39° C at any time in the beginning or during follow
up, do CBC and urine analysis and CRP. If they are abnormal do
blood culture, start antibiotics and decide further treatment based on
blood culture reports.
3. Above 3 years After 3 years of age incidence of occult bacteremia
dramatically declines, often they present with focus of infection. Hence
they need antibiotics, only when they are toxic or present with focus
of infection. In all febrile children irrespective of age group, when
they present with toxic appearance plan, hospitalization, investigation
and antibiotics preferably parenteral.

Prolonged Fever
Fever lasting more than one week with some localizing signs belongs
to this group and common causes are:
• Complicated respiratory infection, such as sinusitis (incompletely
resolved URI with purulent nasal discharge or postnasal discharge,
fever, cough and headache) Pneumonia, empyema.
• Enteric fever
• Malaria
• Urinary tract infection
• Leptospirosis
• Tuberculosis
• Malignancy, like leukemia.
70 Selected Topics in Pediatrics for Practitioners

Short-term Fever—Algorithm

< 30 days of age 30 days to 3 months

Antibiotics, investigate
hospitalise if needed If toxic Non-toxic
Hospitalise

Low risk lab criteria Highrisk lab criteria

(CBC, CRP, urinalysis)

Follow up Antibiotics
as outpatient Investigate
Follow-up for need for
hospitalisation

3 months to 36 months

If toxic Non-toxic
hospitalize

Temperature < 39o C > 39o C (core)

Follow up as
out patient
Low risk lab criteria High risk lab criteria
(CBC, CRP, urinalysis)

Follow up as Antibiotics, need for

outpatient Hospitalization based on
severity and further
investigations

Pyrexia of Unknown Origin (PUO)

Fever documented and no cause identified after one-week evaluation in
a hospital or after 3 weeks of evaluation as an outpatient, no localising
clinical signs or failure of simple diagnostic efforts to identify a cause
are features of this category.

Causes
• Atypical presentations of common illnesses like typhoid, malaria,
leptospirosis or urinary tract infection.
• Unusual infections like brucellosis, infective endocarditis, CMV,
infectious mononucleosis, HIV.
• Malignancy, leukemia, lymphoma.
• Collagen vascular diseases—systemic rheumatoid arthritis, SLE
• Kawasaki’s disease.
 Approach to the Diagnosis and Management of a Febrile Child 71

In this category, tempo of diagnostic evaluation should be adjusted

to the tempo of the illness. In a critically ill child, investigation should
be broad and extensive. Evaluation can proceed gradually stepwise in
a less sick and ambulatory patient.

Recurrent Fever
Here the child is absolutely well between the febrile illnesses.

Common Causes
• Malaria
• Urinary tract infection
• Recurrent URI due to unrelated viruses.

Fever in a High-risk Child

These children are at risk of quick deterioration due to chronic ailments
and prone for unusual viral, fungal or parasitic infection due to immuno-
compromised state.
Hence they need hospitalization, extensive evaluation and broad
spectrum antibiotic therapy. Such common situations are shown below.
• Severe malnutrition
• HIV Positive children
• Asplenia, sickle cell disease
• Immunodeficiency, Immunosuppressive therapy
• Steroid therapy
• Neoplasm and those on chemotherapy
• Chronic respiratory, renal diseases or congenital heart disease.

Non-infectious Causes of Fever

Suspect when the child is well and ambulant and repeated clinical exami-
nations and investigations fail to show any cause.
a. Factitious
b. Metabolic causes—diabetes insipidus, hyperthyroidism.

Management of Fever
Should we have to suppress fever aggressively?
There are arguments both favoring and against using antipyretics.
Against
1. Fever is beneficial to the host, as most of the immune mechanisms
function well, when the temperature is higher then normal.
2. Normalising the temperature is not equivalent to control of infection.
Control of fever may provide a false security.
72 Selected Topics in Pediatrics for Practitioners

For Fever has to be controlled, because it causes dehydration, discomfort

and in some children leads to convulsion.
Considering both arguments, it is prudent to follow a balanced path
in which fever is treated with antipyretics, but less aggressively. This
goal cannot be achieved, unless the parents are educated about the facts
that fever can persist despite antipyretics and it should be accepted in
the absence of serious signs.
Choice of antipyretics Available antipyretics are Paracetamol, Ibuprofen,
Nimesulide and Aspirin. Aspirin is not used in children as antipyretic.
Paracetamol Choice of the drug is mainly decided by safety in addition
to efficacy. Considering the safety profile, wide usage and long experience,
paracetamol is the first antipyretic of choice. It is given in the dose of
10-15 mg /kg every 4-6 hours. In the usual dosage it is safer. Adverse
reactions are rare. Hepatotoxicity is described only in overdosage.
Ibuprofen Used in the dose of 10 mg /kg every 8th hourly. Maximum
recommended dose is 40 mg/kg/day. Adverse effects observed are
nausea, gastritis, skin rash. Gastrointestinal bleeding, hepatic impairment,
renal failure, anaphylaxis and Reye’s syndrome. Advantage of ibuprofen
is that its larger duration of action. But this may not be safer in a child
with situations such as dengue fever.
Nimesulide This is a potent antipyretic at small doses of 5 mg/kg/day
with long duration of action up to 12 hours. It has been found to have
serious side effects such as hypothermia, renal failure and heptotoxicity.
Because of its powerful and prolonged effect, it may mask serious
infection and may provide false security. Control of fever is not equivalent
to control of infection. Simple symptoms like fever need to be treated
by simple and safe drugs. Hence till the safety profile of nimesulide is
clearly established it is better to be avoided.
Dos and don’ts in antipyretic therapy
1. Don’t use fixed dose combinations, as the frequency of dosing may
be different.
2. Don’t alternate two antipyretic drugs such as alternating paracetamol
with ibuprofen at 4 hours interval.
3. Don’t use antipyretics available in combination with decongestants,
antihistamine, metoclopropamide glutathione, etc.
4. Don’t use antipyretic more frequency than that is recommended.
Educate the parents that control of fever does not mean recovery
from infection. They should understand the fact that fever can persist
despite antipyretics in the initial 2 or 3 days and it can be accepted
when there are no danger signs.
 Approach to the Diagnosis and Management of a Febrile Child 73

5. Parenteral preparation of antipyretics does not confer any extra benefit

over oral preparation. Suppositaries may be useful when the child
has intractable vomiting or prone for febrile seizures.
6. Don’t use iced water or eu de cologne for sponging.

Nonpharmacological Methods
Nonpharmacological methods are only adjuncts to drug therapy.
1. Use minimal clothing which will help heat dissemination from body,
unless the child is shivering when they need to be covered up.
2. Make sure that room is well ventilated and fans are switched on.
3. Wipe with tepid water(Just warm or water at room temperature) and
let the water evaporate from the skin. Don’t use cold water which
will cause shivering and may increase temperature.
4. Encourage the child to drink liquids.

Parent Education
Following are the danger signs to be observed in a febrile child, presence
of which is indicative of serious illness. This should be particularly
observed, when the fever subsides, that is between the febrile episodes
1. Young child with age less than 3 months.
2. Unconsolable cry, refusal of feeds, affected by bright light,presence
of stiff neck, lethargy or convulsions.
3. Red spots or patches, coldness of limbs.
4. Breathing difficulty.
5. Continued vomiting, diarrhea.
In a short term fever of less than one week duration, absence of red
flag signs will be reassuring, but anyhow daily monitoring is needed.
 7
Newer Concepts in
Epilepsy Management
G Kumaresan

There has been tremendous advances in the management of epilepsies

in children. There are many new drugs introduced in the last few years.
Recent advances in neuroimaging has led to better understanding of the
etiology of seizures.
The first major advance is in the classification of epilepsies. Epileptic
syndromes is the recent concept wherein a child’s clinical condition is
classified based on the age of onset, clinical type of seizure and the EEG
findings into a epileptic syndrome. This classification helps in selection
of drugs, planning of investigations and in predicting the prognosis.
Examples of such epileptic syndromes include benign conditions like
rolandic epilepsy to more serious conditions like infantile spasms. This
attempt to classify epilepsy into epileptic syndromes is at present
incomplete and in many cases it may not be possible and the old
classification has to be used. In the classification etiologically three
categories are recognized as idiopathic, symptomatic and cryptogenic.
Better understandings about prognosis has been possible in the recent
years with better follow up. Young age of onset, multiple types of seizures,
abnormal background in the EEG and poor early control of seizures are
known risk factors. About 75 percent of children can get a total or
satisfactory seizure control. In about 25 percent the seizure are difficult
to treat and are called intractable seizures. We will see them a little later.
There is a clear consensus in the steps involved in the treatment of
epilepsies. The first step is to differentiate epilepsy from conditions
mimicking epilepsy. Movement disorders, disorders of sleep
breathholding spells and psychogenic seizures can be mistaken wrongly
as epilepsy and treated unnecessarily with anticonvulsants drugs and
lead to poor results and mistaken as intractable seizures.
The next step would be to decide as to whether the seizure is really
an epilepsy. The risk for recurrence has to be evaluated. The seizure has
to be recognized as to whether it is provoked or unprovoked seizure.
If it is a provoked seizure whether prevention of provocative factor may
be sufficient to prevent recurrence of seizures. Examples would include
 Newer Concepts in Epilepsy Management 75

febrile fits and reflex epilepsies. The next step would be to weigh the
risk of recurrence versus the side effects before initiating therapy. There
is a better understanding of the side effects of anti-convulsants on learning
and behavior. This is an important factor to be kept in mind before
deciding on selecting the drug.
The next important concept in the therapy is the importance of mono-
therapy. It is well established that nearly two-thirds of the children can
be controlled with single drug. The concept of drugs interaction between
two anti-convulsants and other drugs have helped us to decide which
combination of drugs are ideal when polytherapy becomes unavoidable.
There are standard references regarding drug interactions. The drug
assay of antiepileptic drugs is the next important advancement in the
therapy of epilepsy. From the initial enthusiasm leading to routine drug
assay in every epileptic child, the indications have settled down to a few
selected indications like:
a. Checking the compliance
b. In the background of systemic illnesses like hepatic or renal diseases.
c. Pregnancy
d. Mentally retarded children
e. Acutely ill child in intensive care unit.
Various characteristic of an individual drug like half life, plasma
binding, mode of excretion have to be considered in every drug used.
The next change in concept is regarding the duration of therapy.
Initially 5-7 years were considered in every patient. Now in many children
withdrawal of drugs after 2-3 fit free years is considered adequate.
However, it is also recognized that the recurrence risk can be as high as
30 percent when these children are followed up. The risk factors are well
recognized and include certain epileptic syndromes, neurological deficits,
mental retardation.
Anticonvulsants which are available can be classified as primary anti
convulsants drugs and newer drugs.
Details of the primary drugs are given in the Table. A few relevant
details of commonly used drugs are given below.
Drug Dosage Strength available Side effects
kg/day in market

Sodium 10-40 mg Syrup 200 mg/5 ml Hepatotoxicity, platelet dysfunction

7 Valproate 250 mg/5 ml obesity, increased appetite, alopecia,
100, 125, 200, 300, pancreatitis, neural tube defects
500 mg tablets
Carbamazepine 20 mg Syrup 100 mg/5 ml Steven Johnson syndrome, anemia,
100, 200, 400 mg ataxia, may aggravate simple absence
tablets and myoclonic jerks

Contd...
76 Selected Topics in Pediatrics for Practitioners

Contd...

Drug Dosage Strength Side effects

kg/day in market

Phenytoin 6-8 mg Syrup 30 mg/5 ml Ataxia, Gingival hyperplasia, hirsutism,

and 100 mg/4 ml, 50, megaloblastic anemia, lymph-
100, mg tablets adenopathy. Not effective in myoclonic
jerks and febrile fits
Phenobarbital 3-5 mg Syrup 20 mg/5 m 15, Hyperactivity, behavioral problems,
30 and 60 mg tablets Because of this, not recommended in
developed countries
Clonazepam 0.1-0.2 mg 0.05, 0.1, 2.0 mg Excessive secretion of saliva and
tablets bronchial secretions, sedation,
hypotonia
Lamotrigine 5-8 mg 25, 50, 100 mg Drug rash
tablets
Vigabatrine 25-50 mg 500 mg tablets Visual disturbances
Topiramate 1-5 mg 25, 50, 100 mg tablets Renal stones

ACTH Injection
150 mg/square meter body surface area [1-3 IU/kg] for first week 75
mg/square meter for 1 week and then on alternate days and then once
a week and taper Acetazolamide 10-20 mg/kg in divided dose.
There is a clear protocol for evaluation of intractable epilepsy. These
children need a comprehensive review, which would include:
a. Whether the diagnosis is correct.
b. Whether the correct drug is given in the adequate dose.
c. Whether structural or neuro-degenerated diseases have been excluded.
The incidence of intractable epilepsy is as high as 25 percent. There
are three avenues for these children.
a. Newer anti-convulsants
b. Surgery for epilepsy
c. Non-pharmocological methods.

Newer Anticonvulsants
In the last 10 years many new drugs have been introduced in the market
and are in various stages of clinical trial. These include:

Levetiracetam/Tigabine, Zonisamide Felbamate

In general newer convulsants are expensive. The knowledge about their
side effects is not complete and have to be tried only after adequate trial
with well established primary drugs. These drugs are used preferably
in consultation with specialist in that field of epilepsy.
 Newer Concepts in Epilepsy Management 77

Non-pharmacological method which has become popular again is

ketogenic diet. This is useful in resistant seizures in children. At present
they can be tried only in selected centers with experience in this field.
The other non-pharmacological method which is gaining popularity is
vagal nerve stimulation. This is useful for children who are unfit for
epileptic surgery. At present, the cost and restricted availability of centers
doing this form of surgery are the limiting factors.
Epileptic surgery has remerged with improvements in imaging
techniques. Video EEGs have led to recognition of frontal lobe seizures.
Many of them were mistaken earlier for pseudo seizures. Ambulatory
EEG and depth electrode recordings have helped to delineate the epileptic
focus more clearly leading to more precise epileptic surgery with good
results.
Advances in MRI techniques, including volumetric analysis have led
to recognition of conditions like mesial temporal sclerosis, neuronal
migration disorders which are amenable to surgery. The concept of
epileptic surgery has spread to pediatric age groups and early use of
surgery in children will have the beneficial effect in preventing permanent
damage in the life style by improving opportunities in education and
employment.
The concept of early surgery has been extended to conditions like
Sturge Weber syndrome megalencephaly. These conditions are termed
as catastrophic epilepsies and surgery at very age is recommended. The
advances in the field of genetics have been tremendrous leading to
recognition of abnormalities in many types of seizures like juvenile
myoclonic epilepsy and febrile fits. This may lead to more precise
diagnosis of genetic syndromes with epilepsy.
Despites all the advances in epilepsy the exact pathophysiology of
epilepsy is not fully understood. All the drugs only prevent the spread
of epilepsy and do not act directly on the epileptic focus. The impact of
the diseases and the drugs on mood and behavior are complex. This has
led to the development of epilepsy as a separate speciality in the field
of neurosciences.

Selection of Drug
Types of epilepsy Drug

Generalized seizures Sodium valproate, Carbamazepine, Phenyloin, Phenobarbitone

Partial seizures Sodium valproate, Carbamazepine, Phenyloin (There are equally
effective—but phenytoin preferably avoided in adolescent girls)

Myoclonic seizures Sodium valproate, Clonazepam, Lamotrigine, Piracetam

Absence seizures Sodium valproate, Lamotrigine, Phenobarbitone
78 Selected Topics in Pediatrics for Practitioners

BIBLIOGRAPHY
1. Aicardi J, Febrile. Convulsions. In Aicardi J (Ed): Epilepsy in Children (2nd
edn). New York: Raven Press, 1994.
2. John M Pellock. Pediatric Epilepsy Diagnosis and Therapy (2nd edn). NewYork:
Demos Medical Publishing Inc., 2001.
3. Kenneth, Swarman, Stephen Ashwal. Pediatric Neurology—Principle and
Practice (3rd edn). St Louis: Mosby, 1999.
 8
Recent Trends in the Diagnosis
and Management of
Bacterial Meningitis
G Kumaresan

Bacterial meningitis is common in pediatric age group and it is a medical

emergency. Early diagnosis is important to prevent mortality and
minimize morbidity. High index of suspicion is needed. Child, who is
less alert and plays less than usual, is the early warning sign.
Improvement in diagnosis includes advances in diagnostic techniques
and neuroimaging. Conventional CSF analysis includes cell count, gram
stain, biochemistry and culture. However, cell count and biochemistry
findings are non-specific and can occur in a variety of other conditions
and lack diagnostic specificity. Culture of the organism is the gold
standard but culture yield is not consistent and is modified by prior
antibiotic therapy and delay in transport of specimen. Hence, there is
need for other methods to diagnose bacterial meningitis. Improvements
in laboratory diagnosis has lead to the tests to detect small components
of infecting bacteria (antigen), test to detect rise in antibody titres in CSF
and serum (IgM and IgG) and antigen-antibody complex. Latex agglu-
tination tests against common bacterial antigen are useful in bacterial
meningitis. However, they are expensive and not easily available. They
are indicated in partially treated bacterial meningitis and are useful in
retrospective diagnosis. Antibody titres and polymerase chain reaction
are used for confirmation of diagnosis in viral infections and tubercular
infections. Other indirect tests include C-reactive protein to differentiate
bacterial versus viral infection. Neuroimaging techniques like CT scan
brain and ultrasound scan brain are helpful in follow up of pyogenic
meningitis. Complications like subdural effusion, vascular occlusion and
hydrocephalus are detected early by these methods. Small subdural
effusions detected on routine CT scan do not need interference. The
indication for tapping of subdural effusions includes persistent fever,
focal convulsions, vomiting, bulging anterior fontenell.
80 Selected Topics in Pediatrics for Practitioners

The therapy of bacterial meningitis has also seen many changes.

Newer antibiotics especially 3rd generation and 4th generation
cephalosporins has replaced older antibiotics like ampicillin and
chloromycetin and shortened the duration of therapy to 14 days in
many cases. However, it is clear that the antibiotics are not the only
answer or total cure. This has led to the understanding of the damage
due to other mechanisms. Rapid death of bacteria, release of cytotoxic
agents like interleukins, tumor necrosis factor lead to cell damage and
damage to vascular endothelium. The first drug tried in this field was
steroids. Administration of steroids 20 minutes prior to first dose of
antibiotics is shown to reduce the complications in hemophilus influenza
infection, but the efficacy in other types of bacterial infection is not fully
established. Injection dexamethasone 0.15 mg/kg 6th hourly for 2-4
days have been tried by many authors but its routine use is not fully
established. The steroids have to be given at least 15-20 minutes prior
to the first dose of antibiotics. This will prevent damage by cytokines
and tumor necrosis factor. This observation has led us to understand
that the damage in meningitis is caused not only by rapidly multiplying
organisms, but also by the products released by dead bacilli and
mediators of inflammation. Thus the pharmacotherapy of meningitis in
future would include anti-CD 18 monoclonal antibodies, pentoxyphylline,
interleukin 10, fucoidin, thalidomide, non-steroidal anti-inflammatory
drugs, anticytotoxic antibody.
The next important area of concern in bacterial meningitis is the
emergence of resistant strains. While penicillin or ampicillin and
chloromycetin or cephalosporin (3rd generation) offered complete
coverage against all common organisms resistant strains of pneumococal
infection to all above antibiotics has emerged and vancomycin may
have to be used in those areas where resistant strains are prevalent.
While on vancomycin therapy concomitant steroids have to be avoided.
Now there are also clear guidelines in the management:
1. Duration of therapy is for 2 weeks except in neonatal meningitis or
immunocompromised individuals.
2. Routine repeat lumbar puncture is not indicated if clinical improve-
ment is satisfactory. However, in neonates and infancy this may not
be applicable.
3. Follow-up of infants with meningitis should include hearing
evaluation and serial head measurement.
4. Convulsions are common in meningitis. First occurrence of Fits after
72 hours of initiation of therapy is not a good sign. If children recovers
without residual deficit, anticonvulsants can be withdrawn.
5. Fluid electrolyte balance has to be maintained balancing between
inappropriate ADH secretion leading to water intoxication and excess
fluid restriction leading to dehydration.
Recent Trends in the Diagnosis and Management of Bacterial Meningitis 81

6. The initial selection of antibiotics should cover common organisms.

This includes H.influenza, N.meningococci and Listeria monocytogenes.
The last mentioned organism is common in children below 2 months
of age and need addition of ampicilin. In others combination of
ampicillin and chloromycetin or 3rd generation cephalsporins will
be indicated for 2 weeks. In special situation like head injury, post-
operative meningitis and immunocompromised state antibiotics has
to be chosen appropriately.
Advances have also been made in the areas of prevention of
meningitis. Widespread use of H.influenzae vaccine has helped to decrease
its incidence. H.influenzae was one of three common organisms in infancy.
Now if an immunized child develops H.influenzae meningitis immuno-
compromsied state has to be considered. Pneumococcal vaccines are
available and are indicated in children with high risks like splenectomised
children or sickle cell anemia. Contact prophylactic therapy with
rifampicin is used in meningococcal and pneumococcal infection.

BIBLIOGRAPHY
1. JH Menkes. Child Neurology (6th edn).
2. Lippincott Williams and Willkiams, 2000.
3. Meningitis Karen L Roos. BI Publications: Delhi, 1997.
 9
Changing Trends in
Prophylaxis of
Rheumatic Fever
P Sabapathy Raj

Rheumatic fever is a non-suppurative inflammatory disease with protean

manifestations affecting various systems predominantly heart and joints
due to antecedent streptococcal infection.

EPIDEMIOLOGY
Data available over the last 20 years indicate that the prevalence of
rheumatic fever in the most vulnerable age group (5-15 years) is 5.3/
1000 in school children, and there appears to be no obvious decline.
The most common age group involved in 5 to 15 years, peak incidence
being at 8 years and both the sexes are equally affected.
Predisposing factors include low socio-economic status, which predis-
poses to overcrowding, poor nutrition, and poor hygiene leading to low
immunological status and thereby, increasing the susceptibility. A
mendelian recessive pattern has also been suggested as a genetic
predisposition.
The statistics of our own experience in Children’s Hospital, Chennai
of inpatient and outpatient cardiological services given below reveals
that actually there is an alarming increase instead of the expected decline
of RF/RHD.
Year No. of Registered RF/RHD

1980 88
1985 135
1990 182
1995 206
2000 224

ETIOPATHOGENESIS
Certain strains of streptococcal antigens (M-1, 3, 6, 18 and 24) shown
immunological properties of heart valves and cell membrane, and
 Changing Trends in Prophylaxis of Rheumatic Fever 83

antibodies produced against streptococcal antigens cross-react with

cardiac and other tissues producing damage. This response may be
amplified by cell mediated immunity.

CLINICAL FEATURES
Acute rheumatic fever is diagnosed by the use of revised Jones criteria.
These criteria were put forward by Dr T Duckett Jones in 1944, which
were revised once in 1965 and later updated once again in 1992.
The criteria have three groups of important clinical and laboratory
findings.
1. Five major manifestations
2. Minor manifestations
3. Supporting evidence of an antecedent group A streptococcal infection.

MAJOR MANIFESTATIONS
Carditis
Carditis occurs in 50 percent of the patients. The signs of carditis include
some or all of the following in increasing order of severity:
1. Tachycardia (out of proportion to the degree of fever) is common. Its
absence rules out myocarditis.
2. Pericarditis (friction rub, pericardial effusion, chest pain and ECG
changes common) may be present.
3. Valvulitis (a murmur indicating MR and/or AR) is always present,
and if not present then carditis should not be diagnosed. Now echo-
cardiographic examination helps in confirming and evaluating the
severity of myocarditis, the presence and severity of MR and AR and
the presence of pericardial effusion.
4. Cardiomegaly on chest radiograph indicates pancarditis, pericarditis
or congestive heart failure.
5. Clinical signs of CCF (gallop rhythm, distant heart sounds, cardio-
megaly) are indications of severe carditis.

Arthritis
The common manifestations of acute rheumatic fever (70% of cases)
usually involve large joints (knee, ankles, elbows, wrists). Often, more
than one joint, either simultaneously or in succession, is involved with
a characteristic migratory nature of the arthritis, swelling, heat, redness,
severe pain, tenderness, and limitation of motion are common. The
arthritis responds dramatically to salicylate therapy; if the arthritis does
not respond within 48 hours the diagnosis of rheumatic fever is probably
incorrect.
84 Selected Topics in Pediatrics for Practitioners

Sydenham’s Chorea
Sydenham’s Chorea (St Vitus Dance) is found in 15 percent of the patients
with acute rheumatic fever. It occurs more often in prepubertal girls (8-
12 years). It begins with emotional lability and personality changes and
loss of motor coordination invariably appear. Characteristic spontaneous
purposeless movements develop, followed by motor weakness. The
adventitious movement, weakness and hypotonia continue for an average
of 7 months (up to 18 months) before slowly waning in severity.

Erythema Marginatum
Erythema marginatum occurs in fewer than 10 percent of the patients
with acute rheumatic fever, and it is very rarely seen in Indian subconti-
nent. The characteristic nonpruritic serpiginous or annular erythematous
rashes are most prominent on the trunk and inner proximal portions of
the extremities, but never seen on face. The rashes disappear on exposure
to cold and reappear when covered with a warm blanket.

Subcutaneous Nodules
Subcutaneous nodules are found in 2 to 10 percent of the cases. They
are hard, painless, nonpruritic, freely mobile and less than 2 cm in
diameter. They are distributed symmetrically, singly or in clusters over
the extensor surfaces of large and small joints, scalp and along the spine.
They last for weeks and are significantly associated with carditis.

Minor Manifestations
1. Arthralgia refers to a joint pain without the objective changes of
arthritis.
2. Fever (with a temperature usually of at least 39°C) generally is present
early in the course of rheumatic fever.
3. In laboratory findings, acute phase reactants (elevated C-reactive
protein levels and ESR are objective evidences of an inflammatory
process.
4. A prolonged P-R interval on electrocardiogram—is neither specific
for acute rheumatic fever nor an indication of active carditis.

LABORATORY FINDINGS
ESR Abnormal > 30 mm/1 hr
Usual values in RF > 60 mm/1 hr
Affected by
1. Anemia increases ESR
2. CCF decreases ESR
3. Anti-inflammatory drugs suppress ESR
 Changing Trends in Prophylaxis of Rheumatic Fever 85

CRP Not affected by anemia or CCF, Normal 6 mg/dl

ASO Peaks 3-6 weeks, remains for 3-6 months.
Diagnostic value is > 240 in adults, > 320 in children,
Any value above 200 may be taken as positive.
Sample taken at 2 to 4 weeks interval should demonstrative rising
titer.
ASO may be affected by antibiotic usage and steroid adminis-
tration.

Diagnosis
The revised Jones criteria (1992) are used for diagnosis of rheumatic
fever.
Major criteria* Minor criteria

Carditis Fever
Polyarthritis, migratory Arthralgia
Erythema marginatum Elevated acute-phase reactants (erythrocyte
sedimentation rate, C-reactive protein)
Chorea Prolonged PR interval on an electrocardiogram
Subcutaneous nodules
Plus
Evidence of a preceding group A streptococcal infection (culture, rapid antigen, antibody rise/
elevation)

*Two major criteria or one major and two minor criteria plus evidence of a preceding
streptococcal infection indicate a high probability of rheumatic fever. In the three special
categories listed below, the diagnosis of rheumatic fever is acceptable without two major or
one major and two minor criteria. However, only for 1 and 2 can the requirement for evidence
of a preceding streptococcal infection be ignored.
1. Chorea, if other causes have been precluded.
2. Insidious or late onset carditis with no other explanation.
3. Rheumatic recurrence: In patients with documented rheumatic heart disease or prior
rheumatic fever, the present of one major criterion or of fever, arthralgia, or elevated acute-
phase reactants suggests a presumptive diagnosis of recurrence. Evidence of previous
streptococcal infection is needed here.

TREATMENT
Rest
Depends on the presence or absence carditis. Brief bed rest is enough,
if arthritis alone is present. In case of carditis it is preferable to have bed
rest at least till ESR returns to normal and CCF is completely controlled.
86 Selected Topics in Pediatrics for Practitioners

Anti-inflammatory Therapy
Polyarthritis Aspirin 100 mg/kg/day in 4 divided doses for 3 to 5
days
75 mg/kg/day when ESR reaches normal value.
Total duration of therapy can be around 4-8 weeks
depending on clinical response. The serum level of
aspirin is to be around 20 mg/dl.
Mild carditis: Aspirin 100 mg/kg/day in 4 divided doses for 2 to 3
weeks. 75 mg/kg/day once ESR is normal for 6-8 weeks.
Moderate/severe Diagnosis of severe carditis is based on the presence
carditis of
1. Cardiomegaly
2. CCF
3. Both aortic and mitral valve involvement and
4. Clinically evident pericarditis.
Even if only one of them is present, carditis is considered moderate/
severe and steroids are to be administered.
Steroids Prednisolone 2.0 mg/kg/day in 4 divided doses for 2-3 weeks.
Start tapering at the end of 2 weeks and do it over 2-3 weeks to avoid
a rebound.
The steroids may be given twice on daily basis also. Aspirin 75 mg/
kg/day is to be added once the steroids are being tapered off.
Note: Prednisolone is tapered by reducing 5 mg from the total dose
every third day. Total duration of therapy will be around 8 to 12 weeks.

Treatment of Chorea
It is self limiting disease and mild chorea can be treated with diazepam.
Severe disease is treated with Haloperidol 0.5 mg thrice daily up to
2.5 mg thrice daily. In resistant cases sodium valproate 15 mg/kg/day
is useful.

Primary Prevention
Proper identification of children with high risk of RF/RHD should be
done routinely in our practice. Very often sore throat is neglected with
the fond hope of being a self limited disorder. The question is how to
pick out the children at risk for RF/RHD. It has to be at low cost, useful
and enable immediate decision. So as not to postpone the treatment
when required. However, most laboratory tests are highly expensive,
and method of collection etc, have a lot of limitations. Hence clinical
knowledge and experience should be more reliable and a high index of
suspicion is important especially when there is sore throat with joint
 Changing Trends in Prophylaxis of Rheumatic Fever 87

pain affecting the major joints and among the poorer socio-economic
groups in particular whose resistance to infections is very low.

Primary Prevention of Rheumatic Fever

Route of
administration Antibiotic Dose Duration

Intramuscular Benzathine penicillin < 27 kg—6 lakhs units Once

> 27 kg—12 lakhs units Once
Oral Penicillin V Children 250 mg tid 10 days
Adolescents and adults 500 mg tid 10 days
Oral Erythromycin 40 mg/kg/day 10 days

Secondary Prevention
Secondary prophylaxis refers to the prevention of colonization or infection
of the upper respiratory tract with group A β-hemolytic streptococci in
individuals who have already had a previous attack of acute rheumatic
fever.
Route of Antibiotic Dose Duration
administration
Intramuscular Benzathine penicillin 1,200,000 units Every 3-4 weeks
Oral Penicillin V 250 mg Twice daily
Sulfadiazine 500-1000 mg Daily
Erythromycin 250 mg Twice daily

Note: Do not use tetracycline antibiotics

Duration of Secondary Prophylaxis

Category Duration

RHD Lifelong
History of Carditis and no RHD Until 40 years of age
Acute Rheumatic Fever and no carditis Until 21 years or 5 years of age from last attack

Oral penicillin is generally not recommended because of the poor

compliance when compared to long-acting parenteral penicillin which
is effective for 3 weeks. However, parenteral penicillin has got the risk
of anaphylactic shock which is a major contraindication. It is also not
good since school children will not be able to attend hospitals regularly,
and the pain factor is also to be reckoned with. On the other hand,
school teachers and parents can be highly motivated to achieve good
compliance with oral penicillin.
 10
Recent Concepts in the
Management of Congestive
Cardiac Failure
P Sabapathy Raj

Congestive cardiac failure (CCF) is defined as a state in which the heart

cannot deliver an adequate cardiac output to meet the metabolic needs
of the body at normal physiologic venous pressure.

Hemodynamic Classification of CCF

Pathophysiology Example

Volume overload
a. Shunts Structural heart diseases
VSD, PDA,
AVSD—Atrioventricular septal defect, atrioventricular
malformation, unobstructed
TAPVR —total anomalous pulmonary venous return
b. Regurgitant valve lesions Truncus arteriosus (with shunt) AVSD, AR
c. Others Anemia, sepsis

Pressure overload
a. Left sided obstruction Hypoplastic left heart COA, AS
b. Right sided obstruction Severe PS
c. Others Severe hypertension

Myocardial disease
a. Intrinsic Myocarditis, Endocardial
Fibroelastrosis,
cardiomyopathies
b. Metabolic Pompe’s disease, hypoxia, hypoglycemia,
hypocalcemia.

Heart rate
a. Tachyarrhythmias SVT
b. Bradyarrhythmias Complete heart block
 Recent Concepts in the Management of Congestive Cardiac Failure 89

Diagnosis of CCF
Infants In older children
Tachycardia Tachycardia
Tachypnoea Fatigue
Poor feeding Effort intolerance
Sweating on feeding Dyspnoea, Orthopnoea
Irritability Cough
Weak cry Anorexia
Wheezing Abdominal pain
Laboured breathing Raised JVP
Gallop rhythm Hepatomegaly
Hepatomegaly Gallop rhythm
Edema—eyelids Edema
Edema—sacrum Basal rales
Failure to thrive
Plus
Cardiomegaly on chest X-ray (it is invariably present) except restrictive
cardiomyopathy and TAPVC with obstruction.

Treatment
The underlying cause of cardiac failure must be removed and alleviated
if possible.
Bed rest Strict bed rest is rarely necessary except in extreme cases, but
it is important that the child rest often and sleep adequately.
Diet Infants with heart failure may fail to thrive because of increased
metabolic requirements and decreased caloric intake increasing daily
calories is an important aspect of their management. Most older children
can be managed with “no added salt” diets and abstinence from foods
containing large amounts of sodium. A strict extremely low sodium diet
is rarely required.

DRUGS
Diuretics
Patients with mild CCF may respond to a high ceiling diuretic alone
even before digitalization. The most commonly used diuretic is
furosemide.
Loop diuretic 1-2 mg/kg/dose IV tid/bd
1-4 mg/kg/day/tid PO
Causes sodium depletion, potassium loss and hypochloremic alkalosis.
Should be supplemented either with potassium chloride supplementation
90 Selected Topics in Pediatrics for Practitioners

(or) coupled with spironolactone 1-3 mg/kg/dose/bd—PO for the

potassium sparing effect.

Inotropes
Digoxin Dosage PO
Premature 0.02 mg/kg
Full term neonate 0.02-0.03 mg/kg
Infant or child 0.02-0.04 mg/kg
IV Dose is 75% of the oral dose

IV Digitalization
0.03 mg/kg—Loading dose
0.015 mg/kg—Stat
0.0075 mg/kg—after 8 hrs
0.0075 mg/kg—after another 8 hrs
Maintenance dose 0.0075 mg/kg/day. After 12 hrs of the last digitalizing
dose.
Digitalis used with caution in
• Premature neonates
• CCF due to myocarditis
• In the presence of renal dysfunction
Use half of the calculated digitalizing as well as the maintenance
dose initially in these situations.

Dopamine/Dobutamine Infusion
Preparation
Amount of dopamine in mg : 6 × body weight to be reconsti-
tuted upto 100 ml of 5% GDW
Example : 60 mg in 100 ml of 5% GDW
Rate of infusion: 1 ml/hr, : 1 μg/kg/min
e.g. 10 μg/kg/min : 10 ml/hr
Available strength
Dopamine—5 ml = 200 mg
Dobutamine—5 ml = 250 mg

Adrenaline/Noradrenaline Infusion
Preparation
Amount of adrenaline = 0.6 × body weight to be added in 100 ml
of D5/N5
Example : 10 kg Child
 Recent Concepts in the Management of Congestive Cardiac Failure 91

Amount of adrenaline = 10 × 0.6 = 6 mg (6 ml) to be diluted

in 100 ml of D5/N5
Rate of infusion
1 ml/hr = 0.1 μg/kg/min
Adrenaline infusion = 0.1 μg/kg/min raised upto 1 μg/kg/min
Noradrenaline infusion = 0.1 to 2 μg/kg/min
Titrate to desired effect.
Available strength
Adrenaline = 1 mg in 1 ml (1:1000).
Milrinone
It is a phosphodiesterase inhibitor, prevents degradation of cAMP. It has
both positive inotropic effect and peripheral vasodilatory effect. It is
used in treating patients with:
• Low cardiac output refractory to standard therapy.
• Critically ill infants with CCF.
• CCF with renal dysfunction (e.g. COA)
• In postoperative cardiac patients with CCF.
Dose Loading dose 50 μg/kg IV followed by 0.5-0.75 μg/kg/min IV
infusion.
Side effect Hypotension, managed by IV fluid administration.

After Load Reducing Agents

Indicated in
• Large L-R shunt, e.g. VSD, PDA
• Regurgitant lesions, e.g. MR, AR
• Poor systolic function, e.g. myocarditis, dilated cardiomyopathy
• ACE inhibitors are the agents of choice.
Captopril
Mixed vasodilator reduces the systemic vascular resistance by inhibiting
angiotensin II generation and augmenting the production of bradykinin.
Dose
Infants : 0.1-0.5 mg/kg/dose tid
Children : 0.1-0.2 mg/kg/dose tid
Premature : 0.1 mg/kg/dose

Enalapril
Dose 0.8-0.5 mg/kg/dose bd.
Sodium Nitroprusside
Mixed vasodilator. Prepared as an infusion with dextrose containing
solution, should be protected from sunlight. Dose is 0.1 to 1 μg/kg/min
maximum 8 μg/kg/min.
92 Selected Topics in Pediatrics for Practitioners

Watch for Hypotension, methemoglobinemia, hypothyroidism after

high dose and prolonged use. Indicated in cardiogenic shock with
increased systemic vascular resistance, refractory to treatment with
Inotropes alone.

Nitroglycerin
Predominantly venodilator, coronary and pulmonary vasodilator.
Dose 0.5-1 μg/kg/min infusion, light sensitive. Use only if preload is
optimal. Used with Dopamine or Adrenaline infusion in refractory
cardiogenic shock. Look for hypotension, headache.

Beta Blockers
Most useful in patients with dilated cardiomyopathy.

Metaprolol
Selective β1 blocker.
Dose 0.1 mg/kg/dose bd increase to maximum of 0.9 mg/kg/min.

Carvedilol
It is a β and α blocker with free radical scavenging effects. Use in adults
have been promising. Their use in children is under trial.

PGE1
It is indicated when ductal dependent cardiac Alprostadil lesions
are diagnosed or when they cannot be ruled out.
a. Absent femoral pulses
b. The inability to increase the systemic arterial PaO2 to above 150
mmHg with a fraction of FiO2 of 1 suggests ductal dependent lesion.
Here treatment with PGE1 is warranted.
Dose 0.05-0.1 μg/kg/min IV infusion. Maintenance infusion rate is 0.01-
0.05 μg/kg/min.

Long-term Management of CCF

Chronic or Stable CCF If the underlying causes of CCF cannot be imme-
diately corrected in a patient who is hemodynamically stable, outpatient
management can be initiated.
• Nutritional support
• Oral digoxin, maintenance dose 0.005-0.01 mg/kg/day in 2 divided
doses.
• Oral furosemide—1 to 4 mg/kg/24 hrs tid
• Add spironolactone—1 to 3 mg/kg/day/tid PO
 Recent Concepts in the Management of Congestive Cardiac Failure 93

• Potassium supplementation—Potassium chloride 1 to 2 mEq/kg/

day in 3 to 4 divided doses.
• Correct anemia
• Treat the underlying cause.

TREATMENT PROTOCOL OF CONGESTIVE CARDIAC FAILURE

 11
Current Trends in Diagnosis
and Management
of Bronchial Asthma
TU Sukumaran

INTRODUCTION
The word asthma is derived from a Greek word which means ‘shortness
of breath”. Bronchial asthma has emerged as one of the leading causes
of chronic illness in childhood. The disease accounts for a large proportion
of health care spent and time lost from school and work. The progress
in understanding the pathophysiology of the disease over the years has
led to improved therapy and control. But at the same time, it is a matter
of concern that the severity of the disease has increased drastically as
measured by the morbidity and mortility rates. According to various
studied, the prevalence rates range from 0.2 to 25 percent with an
estimated incidence between 2 to 5 cases per 1000 per year among all
age groups.

DEFINITION
In 1991, the National Asthma Education Programme Expert Panel Report
from the National Institute of Health defined asthma as:
A lung disease with the following three characters:
i. Airway obstruction that is reversible, either spontaneously or with
treatment.
ii. Airway inflammation.
iii. Increased airway responsiveness to a variety of stimuli.

Inheritance
The inheritance of asthma is thought to be polygenic and multifactorial.
The genes that have been linked to asthma are those related to atopy.
Though a number of genes have been identified, the two genes that
have been examined in detail are the ones situated on chromosome 11q
and 5 q.
 Current Trends in Diagnosis and Management of Bronchial Asthma 95

Etiopathogenesis
Asthma is a complex disease involving autonomic, humoral, immuno-
logic, infectious, endocrine and psychological factors.
i. The balance between excitatory (cholinergic, α–adrenergic and non-
cholinergic) and inhibitory mechanism (β–adrenergic and non-
adrenergic) is one of the major determinants of airways diameter.
Vasoactive intestinal peptide (VIP) is a bronchodilator while
substance p increases smooth muscle tone.
Humoral factors favoring bronchodilation are endogenous
catecholamines that act on β-adrenergic receptors. Histamine and
leukotrienes produce bronchoconstriction.
ii. Immunological factors Earlier asthma used to be classified into
Extrinsic and Intrinsic asthma.
Extrinsic asthma otherwise known as allergic asthma is charac-
terised by increased concentration of both total IgE and specific
IgE against the particular allergen. Intrinsic asthma being non-IgE
mediated is triggered by infection.
But recent studies refute such a distinction, stating that a
common basic immunological disorder is present in all forms of
the disease, the exact mechanism being unknown.
iii. Viral infections These are the most important triggers of asthma.
Respiratory Syncytial Virus (RSV) and parainfluenzae virus are the
ones implicated in infancy while Rhinoviruses are the major ones
in older children. The exact mechanism by which these agents
initiate an attack is obscure, but it is thought to be through the
stimulation of afferent vagal receptors.
iv. Endocrinal factors It has been found that pregnancy, menstruation
and thyrotoxicosis worsen the disease.
v. Psychological factors Emotional factors are thought to cause broncho-
constriction through the vagal afferents.
vi. Exercise: Exercise triggers asthma by causing dehydration of the
respiratory tract which causes mucosal hyperosmolarity. This
induces the mediator release from mast cells.

Risk Factors
1. Age The risk is increased in the extremes of age. But asthma may
have its onset at any age. Thirty percent of patients are symptomatic
by 1 year of age. Eighty to ninty percent have their first symptom
before 4 to 5 years of age.
2. Sex Before puberty, the boys are twice as affected as compared to
girls. Thereafter the sex incidence is equal.
96 Selected Topics in Pediatrics for Practitioners

Family history A child with one affected parent has about 25 percent
risk of having asthma. If both parents are asthmatic, the risk increases
to 50 percent.
3. Race Asthma is more common in blacks.
4. Socioeconomic status Children belonging to low socioeconomic status
have been found to have a higher risk probably due to the associated
factors like overcrowding, indoor air pollution and allergen exposure.
5. Maternal age Children born to very young mother (< 20 years) are at
a higher risk to develop asthma in later life.
6. Gestational age and birth weight Prematurity and low birth weight
babies have a four-fold increased risk of developing asthma.
7. Maternal smoking
8. Respiratory illness.

Trigger Factors
Inhaled allergens like pollens, mold spores, animal dander, cereal grain
dust, house dust, dust mite (dermatophagoides farinae) and cigarette
smoke. Others include vegetable proteins, viral infections, noxious odour,
air pollutants, drugs (NSAIDs, β receptor antagonists, metabisulfite),
cold air and exercise.

Pathophysiology
The various manifestations of asthma are due to bronchoconstriction,
hypersecretion of mucus, mucosal edema, cellular infiltration and desqua-
mation of epithelial and inflammatory cells.
Atopic individuals are sensitised after exposure to allergens and
develop IgE antibodies. Subsequent exposure to allergens cause a dual
response which is protracted and more severe. There are two responses
to allergic exposure.
1. Early asthmatic response (EAR) Occurs due to the mast cell mediator
release which includes histamine, leukotrienes C4, D4 and E4 (slow
reacting substance of anaphylaxis—SRSA) and platelet activating
factor. This leads on to the Reversible Obstructive Airway Disease
(ROAD) and this immune response is reversible with bronchodilators
and may be prevented by mast cell stabilizing agents.
2. Late asthmatic response This occurs 6 to 8 hours later and is due to T-
cell mediated influx of inflammatory mediators mainly eosinophils.
This produces a continued state of bronchial hyper reactivity (BHR)
due to inflammation. This phase can be treated with antiinflammatory
drugs like steroids. Repeated bronchoscopic evaluation conducted in
1980s have proved that generalised and persistent airway inflam-
mation is the major underlying pathology even in patients with newly
diagnosed and mild asthma.
 Current Trends in Diagnosis and Management of Bronchial Asthma 97

The pathological changes in asthma include bronchoconstriction,

epithelial damage, basement membrane thickening, increase in bronchial
capillary bed, fluid exudation with edema, mucus gland hypertrophy,
bronchial smooth muscle hypertrophy, infiltration of inflammatory cells
and intraluminous mucous and cellular debris. Pathognomomic findings
include Charcot-Leyden crystals (Iysophospholipane from eosinophil
membranes), Curshmann spirals (bronchial mucus casts) and Creola
bodies (desquamated epithelial cells).

Physiological and Functional Alterations in Asthma

1. Reversible airway obstruction
2. Reversible hyperreactivity
3. Dynamic hyperinflation
4. Ventilation perfusion abnormalities and
5. Finally irreversible airway obstruction.

Diagnosis
The constellation of points got from the history, the clinical features and
presentation, confirmed by pulmonary function tests clinches the diag-
nosis of asthma.

History
There is usually a history of exposure to an allergen or a viral infection.
Detailed history should be taken regarding the severity and frequency
of the symptoms. Enquiries should be made about the presence of
nocturnal symptoms which typically occur around 3 AM and responds
well to bronchodilators. A meticulous history may help us to narrow
down the possible allergen. Family history for presence of atopy or
asthma should be sought.

Clinical Features
Symptoms
Wheezing, dyspnoea cough and sensation of tightness in the chest are
the main complaints during an acute attack.
Cough is usually non-productive early in the course of an attack.
Abdominal pain is common in children due to the strenuous use of
abdominal muscles including diaphram.
Vomiting is another associated symptoms.
Signs include tachypnoea, tachycardia, pulsus paradoxus, cyanosis,
hyperinflation of chest, use of accessory muscles of respiration,
98 Selected Topics in Pediatrics for Practitioners

hyperresonance on percussion, prolongation of expiration and the charac-

teristic polyphonic wheeze on auscultation.
With severe obstruction, the child may assume a hunched over tripod
like sitting position that makes it easier to breathe. At this stage, the
characteristic wheeze may disappear leading to the ominous “silent
chest” which is a medical emergency.

Guidelines for Diagnosis of Bronchial Asthma

Diagnosis is mainly clinical and should be considered when:
1. More than 3 episodes of symptomatic airflow obstruction occurs
2. Airway obstruction is at least partially reversible and
3. Alternative causes of wheezing are excluded.

INVESTIGATIONS
Blood examination Peripheral smear may show eosinophils. Absolute
eosinophilia in the range of 2500 cells/ml is usually seen in patients
untreated with steroids and correlates well with the severity of the
disease.
Sputum examination May reveal eosinophils, creola bodies, Charcot–
Leyden crystals and Curshmann’s spirals. Gram staining for microbes
may be done if there is super added infections.

Chest X-ray
Usually normal in majority of uncomplicated asthmatics. In others it
may show emphysematous changes. It helps to rule out tuberculosis.

PULMONARY FUNCTION TESTS INCLUDE

i. Peak expiratory flow rate (PEFR)
ii. Spirometry.

Peak Expiratory Flow Rate (PEFR)

This is an easy procedure and can be performed in children above 6
years.
PEFR is the fastest rate at which air can more through the airways
during a forced expiration starting with fully inflated lungs. The PEFR
correlates well with FeV1. It is measured with the help of a peak flow
meter. PEFR should be measured at least twice a day–morning and
evening. The peak flow varies according to age, sex and height.
 Current Trends in Diagnosis and Management of Bronchial Asthma 99

Uses of PEFR Recording in Asthma

1. Quick diagnosis and assessment of asthma
Findings suggestive of asthma include:
i. It there is a 15 to 20 percent increase in the peak flow after adminis-
tration of a bronchodilator. It indicates a significant degree of
reversible airway obstruction.
ii. Diurnal variation of > 20 percent.
iii. < 80 percent predicted value.
2. When taken regularly, can give a warning of an impending attack
as characterised by a fall in PEFR. Helps in monitoring the
effectiveness of the treatment.
3. Long-term follow-up This is done by comparing the PEFR with
one’s personal best (PB) peak flow. The personal best peak flow is the
highest measurement that can be achieved in the middle of a good
(asymptomatic) day after using initiated bronchodilator. Values
persistently below 20–30 percent of the personal best would indicate
worsening control.
4. Helps in decision making with regard to discharge from hospital.
If diurnal variability is more than 20 percent discharge is not advisable.

Spirometry
Role of spirometry is limited in our set up. It is, cumbersome and is
available only in few centres.
A ratio of FeV1/FVC of less than 80 percent indicates airflow
obstruction. Also a reversibility in the absolute value of FeV1 by more
than 20 percent after bronchodilator indicates a significant reversible
airflow obstruction.

DIFFERENTIAL DIAGNOSIS
Birth to Six-months (Seldom Asthma)
i. Bronchiolitis Characterised by a short prodrome like fever, upper
respiratory or gastrointestinal symptoms. Usually restricted to a
single attack. There are signs of respiratory distress and fine crackles
in the chest. Liver and spleen are pushed down due to the hyper-
inflation.
ii. Aspiration syndromes The presence of choking episodes, vomiting
and symptoms related to feeding should rise suspicion of aspiration.
iii. Congenital heart disease Features may include tachypnea, feeding
difficulties, excessive sweating, cyanosis, heart murmurs and other
features of heart failure. An echocardiography will help in confir-
ming the diagnosis.
100 Selected Topics in Pediatrics for Practitioners

6 months to 3 Years (Asthma Probable)

i. Bronchiolitis.
ii. Transient wheezing of childhood (TWC). There are recurrent
episodes of wheezing, associated with fever. Then is no personal
or family history of atopies.
iii. Early onset asthma.
iv. Foreign body inhalation: Usually there is a typical history of
aspiration in recent past. The wheeze and other respiratory signs
are localised. Bronchoscopy is indicated.
v. Congenital heart disease.
vi. Infections, e.g. TB

Late Childhood > 3 Years

Most likely asthma. Differential diagnosis include TWC, foreign body
aspiration, CHD, and infections (of sinuses, adenoids, TB). Another
differential diagnosis is congenital malformations causing airway
obstructions like vascular rings, bronchogenic cysts and tracheomalacia.
An X–ray or CT scan can detect these abnormalities.

MANAGEMENT OF BRONCHIAL ASTHMA

Acute and Acute Severe Bronchial Asthma
Parents and physicians should learn to recognise acute asthma in its
early stage. With progression of acute attack, the reversibility of airway
obstruction in response to β2 agonists and other bronchodilators becomes
diminished. This is the result of airway narrowing caused by mucosal
oedema and mucus plugging.
During an acute attack enquire the following:
• Precipitant or trigger factors.
• Duration of attack.
• Response to previous treatment.
• Time and dose of last theophylline.
• Brittleness (rapid worsening after onset).
• Number and severity of previous attacks.

RECOGNITION OF SEVERITY OF ASTHMA

Severe bronchial asthma is characterised by:
• Too breathless to feed
• Respiratory rate > 50/minutes
• Heart rate > 140/minutes
• PEFR < 50 percent of the best
 Current Trends in Diagnosis and Management of Bronchial Asthma 101

• Poor or only transient (< 2 hours) response to bronchodilator.

• Worsening despite 2-3 rescue doses of bronchodilator at 15 minutes
interval.

LIFE-THREATENING ASTHMA IS CHARACTERIZED

• Unable to talk or cry
• Cyanosis
• Feeble chest movements
• Absent breath sounds
• Fatigue or exhausted
• Agitated
• Altered sensorium
• Oxygen saturation < 91 percent in pulse oximeter.
Assessment of severity of an acute attack of bronchial asthma can be
done by a simple scoring system called pulmonary score index (PSI).

Pulmonary Score Index (PSI)

Score Respiratory rate Wheezing Accessory muscle—

< 6years > 6 years Sternomastoid activity

0 < 30 < 20 None No apparent activity

1 31-45 21-35 Terminal expiration Questionable increase
with stethoscope
2 46-60 36-50 Entire expiration with Increase apparent
stethoscope
3 > 60 > 50 During inspiration Maximal activity
and expiration
without stethoscope

Score 0–3 Mild If no wheezing due to minimal air exchange score–3

4–6 moderate
> 6 severe

Those children whose score is > 6 should be admitted to a paediatric

ICU.

MANAGEMENT
• Oxygen
• Nebulised β agonist, intravenous β-agonist
• Anticholinergic drugs
• Steroids
• Magnesium sulphate
• IV aminophylline
• Isoproterenol
102 Selected Topics in Pediatrics for Practitioners

OXYGEN
• Hypoxia is due to ventilation–perfusion mismatch.
• β–agonists may increase hypoxia by attenuating the hypoxic
pulmonary vasoconstriction, hence oxygen should always be adminis-
tered along with nebulised β-agonist.
• Maintain oxygen saturation between 90–95 percent.

NEBULISED β AGONISTS
• β-agonists are drugs of choice in asthma.
• Patients with acute severe asthma require and tolerate higher doses.
• Dose 0.15 mg/kg, minimum 0.25 ml < 6 month, 0.5 ml > 6 month,
0.5 to 1 ml older children and adults.
• Dilute in normal saline only, never distilled water.
• All patients should receive 3 nebulizations at 20 minute intervals
with oxygen and ECG monitoring.
• Continuous nebulized salbutamol 10 mg in 7-10 ml saline may be
administered via a jet nebulizer if symptoms persist.
• Failure to respond to high dose β-agonists is an indication for ICU
admission and re-evaluation of diagnosis.

STEROIDS
• Steroids directly reduce inflammation in this predominantly
inflammatory illness.
• Should be used early in all patients with acute severe asthma. Under
use of steroids has been incriminated in fatal cases.
• Oral steroids may cause vomiting, hence hydrocortisone or methyl-
prednisolone (MPS) may be administered IV.
• Dose MPS 2mg/kg stat followed by 1mg/kg Q6H or Hydrocortisone
10 mg/kg stat followed by 5 mg/kg Q6H.
• IV steroids may be stopped after 48 hours or after improvement
commences.
• Inhaled steroids unlikely to be of benefit in the acute episode.

ANTICHOLINERGIC AGENTS: IPRATROPIUM

• Useful as an adjunct with salbutamol in the acute episode, less effective
alone.
• Dose < 1 year to 0.5 ml, > 1 year–1 ml
• Has longer duration of action and less systemic side effects compared
to atropine.
 Current Trends in Diagnosis and Management of Bronchial Asthma 103

INTRAVENOUS β2 AGONISTS
• IV terbutaline or IV salbutamol may be used if patient fails to improve
with nebulized β2 agonists.
• Dose Terbutaline: Initial bolus of 5 to 10 μg/kg over 10 minutes
followed by 2-10 μg/kg/hour.
• Higher infusion rates may be used with caution.
• Continuous ECG monitoring of the heart rate, rhythm and ST segment
changes. If HR > 180/minute, arrhythmias or ST changes develop,
dose of β-agonists should be halved.
• Discontinue nebulization at higher infusion rate or if signs of toxicity
develop.
• Preparation of terbutaline 1 ampoule (1 ml) contains 500 μg dissolve 1
ampoule in 50 ml of 5 percent dextrose so that 1 ml = 10 μg terbutaline.

MAGNESIUM SULPHATE
– Useful in severe asthmatic.
– Mechanism Calcium channel modulation resulting in decreased
acetyl chloline and histamine release.
– Efficacy, dose and frequency have not been clearly worked out.
– Suggested dose 25–50 mg/kg to be diluted in N. saline and adminis-
tered as an infusion over ½ hour.
– Side effects Tachycardia/bradycardia, hypotension, muscle weak-
ness at higher serum levels.

AMINOPHYLLINE
– Doubtful additional bronchodilatation if optimal β agonists used.
– Possible role in improving diaphragmatic contractility and
inflammatory modulation may confer additional benefit.
– Dose Loading dose 5 to 10 mg/kg/hr followed by 0.5-1.0 mg/kg/
hr.
– Avoid loading dose if patient is already receiving theophylline.
– Dose of terbutaline to be decreased by 50 percent when concur-
rently infused with aminophylline.
– Monitor levels if possible, keep between 10 to 20 mg/dl. Watch
for drug interactions-anticonvulsants, (decrease levels), H 2
blockers, macrolides (increase levels). Infections, especially viral
also modify theophylline levels.
– Toxicity–GI (vomiting, gastritis), cardiac (tachycardia, arrhy-
thmias), CNS (irritability, seizures).
104 Selected Topics in Pediatrics for Practitioners

ISOPROTERENOL
– Synthetic agent with pure β1 β2 effects.
– Powerful bronchodilator, sometimes used as ‘last–ditch effort’
when need for ventilation appears imminent.
– Reports of fatal myocardial necrosis have decreased popularity of
this agent.
– Dose Continuous infusion of 0.05 to 0.1 μg/kg/minute

Supportive Care
Adequate hydration–may need more than maintenance initially due to
extra insensible losses, remember to cut down when ventilated. Watch
for SIADH, especially on positive pressure ventilation.

Antibiotics
Not routinely indicated. Some use prophylactic antibiotics, especially in
presence of significant mucus plugging.

Indications for Intubation

Absolute
• Cardiac arrest
• Comatose child
• Severe respiratory distress
• Silent chest, exhaustion

Relative
• Hypoxemia pO2 < 60 mmHg in
60 percent oxygen
• pCO2 > 65 mmHg and or pCO2
Rising by > 5 mmHg/hr
• Metabolic acidosis (–BE > 8–10)

Intubation
Need for intubation and assisted ventilation in acute asthma is infrequent
in most centres. Intubation of a refractory asthmatic with respiratory
failure may pose considerable risks as:
– Pre-existing hypoxemia and acidosis may be further aggravated
– Vagal stimulation during laryngoscopy may potentiate broncho-
spasm.
Hence intubation of the asthmatic should be done by a skilled and
experienced physician. Nasotracheal tubes generally preferred as they
are more comfortable for the patient.
 Current Trends in Diagnosis and Management of Bronchial Asthma 105

DRUGS USED DURING INTUBATION

Sedation options—Ketamine (+ antisialogogue) and midazolam/fentanyl
paralyse with vecuronium, spray vocal cords with ½ cc of 2 percent
lignocaine prior to intubation.

Ventilation
Modes and setting should have the ability to deliver constant tidal
volumes in the face of changing airway resistance and cater to the long
time constants in these patients.
Suggested settings Volume limited ventilation with high flow rates assures
constant tidal volume. Slow rates and long I: E rations in order to give
enough time for exhalation and minimize air trapping.
Low PEEP 1 to 2 cm H2O, however PEEP may be increased (3-5 cm)
during weaning.
It is important to limit plateau pressures to < 35 cm H2O, in order
to minimize risk of barotrauma.
Alternative strategy in severe asthmatic with plateau pressures > 35
cm with above settings is controlled hypoventilation or “permissive
hypercapnia”, where hypoxia is corrected but not hypercapnia. Here
tidal volumes are limited to 5 to 7 ml/kg and resulting respiratory
aciodosis is controlled with sodium bicarbonate if pH < 7.1 to 7.2.
Flow volume loops may be followed on the ventilator in order to
limit auto–PEEP and dynamic hyperinflation.
Child should be sedated with fentanyl and midazolam or ketamine
(sedative agent with bronchodilatory properties).
In addition, muscle paralysis is preferred at least during first 24
hours of ventilation as a struggling child may cause airway resistance
to be dangerously elevated.
β-agonists should be continued during ventilation preferably
nebulized into the ventilatory circuit or via the intravenous route.

CRITERIA FOR WEANING

• Clinical improvement in bronchospasm
• Inspiratory pressures of < 30 to 35 cm H2O
• Normal gases in 40 percent oxygen
• CXR showing reduced hyperinflation.
Note All possible measures to be taken to prevent intubation and
mechanical ventilation.

Post ICU Plan, Prevention of Future Status

There should be an effective discussion with the family on possible
reasons for the current status attack. Effective use of anti-inflammatory
106 Selected Topics in Pediatrics for Practitioners

therapy and bronchodilator therapy should be emphasised, and a written

plan for future acute attacks should be given to the care–giver.

Algorithm for Management of Acute Severe Asthma

1. Establish diagnosis, consider differential diagnosis particularly if first
presentation.
2. Assess severity.

Initial Treatment
• Oxygen to maintain saturation > 90-95 percent
• Nebulized salbutamol 3 doses at 20 minute intervals
< 20 kg—0.5 ml salbutamol with 3 ml N Saline
> 20 kg—1 ml salbutamol with 3 ml N Saline
• Nebulized ipratropium—< 1 year—0.5 ml, > 1 year—1 ml
• Steroids: Methylprednisolone 2 mg/kg stat, followed by 1 mg/kg
Q6H or Hydrocortisone—10 mg/kg stat followed by 5 mg/kg × 6th
hourly daily.
 Current Trends in Diagnosis and Management of Bronchial Asthma 107

MANAGEMENT OF PERSISTENT BRONCHIAL ASTHMA

Children with persistent bronchial asthma (same as chronic bronchial
asthma) can be classified into 4 groups—mild intermittent, mild
persistent, moderate persistent and severe persistent bronchial asthma.
This classification is depending on frequency of day time attacks, night
symptoms, restriction of physical activity and PEFR.
For prevention of bronchial asthma, one should remember 4Ps—
pharmacotherapy using preventors, prevention of trigger factors, parent
education and peak expiratory flow rate monitoring.

INHALED STEROIDS—THE FIRST LINE TREATMENT

It would seem misappropriate to treat bronchial asthma with beta agonist
alone since these agents do not control the fundamental inflammatory
process of bronchial asthma. Thus, though beta agonist are very effective
at providing immediate bronchodilatation and relieving symptoms, they
have no effect on the cells that mediate chronic inflammation resulting
in airway hyper-responsiveness. It follows that asthma should be
controlled by inhibiting inflammation. This is best achieved with inhaled
steroids, which are most effective as well as the safest drugs to control
the disease. Inhaled steroids are used as first line treatment for any
patient with persistent bronchial asthma. Patients who need to use short
acting inhaled β2 agonists more than thrice a week are candidates for
inhaled steroids. This approach has been shown to markedly reduce
asthma morbidity in terms of reducing symptoms and preventing
exacerbations. Inhaled steroids also significantly improve the quality of
life, which means that children can lead normal life, and can participate
in sports, which would have been otherwise avoided due to fear of
triggering exercise induced bronchial asthma. The widespread use of
steroids has probably reduced bronchial asthma mortality also. It has
been recently recognised that inhaled steroids not only control the disease,
but may also prevent irreversible changes in lung function resulting
from uncontrolled chronic inflammation.

INHALED STEROIDS: TREATMENT STRATEGIES

Three dose categories of BPD/BUD may be used for increasingly severe
disease—low dose (< 400 mcg), medium dose (400-800 mcg) and high
dose (> 800 mcg). The corresponding doses for FP are half those of BPD/
BUD using similar delivery system.
In step care approach children with increasing level of severity are
maintained on ascending grades of therapy. Treatment may start at a
108 Selected Topics in Pediatrics for Practitioners

step determined by patient’s severity of asthma and be gradually ‘stepped

up if necessary. Alternately it may start at a higher level to provide rapid
relief and then be ‘stepped down’ for achieving control. The latter
approach is favoured by the fact that the patient witnesses rapid results,
thus gaining confidence and leading to better compliance. If child has
been well controlled at any step for 3–6 months, stepping down one
level at a time should be considered. If on inhaled steroids, the dose
should be reduced by 25 to 50 percent at each visit.

Step-wise Increase (Guideline)

• Start with estimated dose
• Increase the dose if control is not achieved.

Start High–go Slow

• Start with high dose (800 mcg/day)
• Reduce dose once control is achieved
• Maintain on lowest possible dose.

Step Down of Inhaled Steroids

• Step down when asthma is controlled
— No symptoms
— Optimal lung function
— Infrequent inhaled β2 agonist use.
• Reduce dose by 25 percent by 3 months.
• Duration of treatment—controversial. Can be continued for three
years without systemic side effects of steroids.
• Some patients may be able to discontinue inhaled steroids.

Treatment in the Step-wise Approach

to Long-term Management of Asthma
The aim of treatment is control of asthma:
• Minimal (ideally no) chronic symptoms, including nocturnal symp-
toms.
• No emergency visits.
• No limitation of activities, including exercise.
• (Near) normal PEFR.
• Minimal (infrequent) episodes.
• Minimal need for β2 agonist.
• PEFR variability < 20 percent.
• Minimal (or no) adverse effects from medicine.
 Current Trends in Diagnosis and Management of Bronchial Asthma 109

Before Starting Treatment, Classify the Severity at Presentation

Intermittent Persistent

Category Mild Mild Moderate Severe

Symptoms I II III IV

Day-time < 1 time a week > 1 time a week Daily Continuous limited
symptoms Asymptomatic but < 1 time a day Use β2 physical activity
and normal PEFR agonist; daily
between attacks attacks affect
activity

Night-time < 2 times a > 2 times a month > 1 time a Frequent

symptoms month week
PEFR > 80% predicted > 80% predicted > 60-80% < 60% predicted
(predicted) variability < 20% variability 20–30% predicted variability > 30%
variability
> 30%

Global initiative for asthma (GINA) WHO/NHLBI, 2002

Global Initiative for Asthma (GINA) Revised—2002

Recommended Medication by Level of Severity

Step 1 Step 2 Step 3 Step 4

Intermittent Mild persistent Moderate Severe persistent asthma

asthma asthma persistent
asthma

Daily controller Daily controller Daily controller Daily controller medications

medications medications medications

None necessary Inhaled Inhaled Inhaled glucocorticosteroid

glucocorticosteroid glucocorticosteroid (800 μg budesonide or equivalent)
(100-400 μg (400-800 μg plus one or more of the following
budesonide or budesonide if needed
equivalent) or equivalent)
Other treatment Other treatment
options options
Sustained-release Inhaled Sustained-release theophylline
theophylline, or glucocortico- Long–acting oral β2-agonist
Cromone, or steroid (< 800 μg Leukotriene modifier
Leukotriene budesonide
modifier or equivalent) Oral glucocorticosteroid
plus
sustained–release
theophylline, or

Contd...
110 Selected Topics in Pediatrics for Practitioners

Contd...

Step 1 Step 2 Step 3 Step 4

Inhaled
glucocorticosteroid
(< 800 μg budesonide
or equivalent) plus
Long-acting
inhaled β2-agonist,
or
Inhaled
glucocorticosteroid
(< 800 μg budesonide
or equivalent) plus
leukotriene
modifier

Children with intermittent asthma but severe exacerbations should

be treated as having moderate persistent asthma.

All Steps
Once control of asthma is achieved and maintained for at least 3 months.
a gradual reduction of the maintenance therapy should be tried in order
to identify the minimum therapy required to maintain control.

Notes

Step-down Step-up

Review treatment every 3-6 months If control is not achieved, consider step-up. But first:
If control is sustained for at least review patient medication technique, compliance, and
3 months, a gradual stepwise environmental control (avoidance of allergens or other
reduction in treatment may be trigger factors)
possible

PREVENTION OF ASTHMA: AVOIDANCE OF TRIGGER FACTORS

Allergen Avoidance
Indoor Allergens
Cockroach, house dust mite, fungal spores, animals (pets) are the main
source and skin testing can be used for the diagnosis. The following
control measures are suggested.
Cockroaches Leave no food uncovered. Traps to catch cockroaches are
better than anticockroach chemicals.
House dust mite Sun the bedding weekly. No carpets or stuffed,
upholstered furniture in the house. The mattresses and pillows should
 Current Trends in Diagnosis and Management of Bronchial Asthma 111

be covered with impervious coverings. Proper mapping of the country

needs to be done to see where house dust mite is an important allergen
(expected in warm, humid climate).
Pets Pets like dogs, cats or birds should not be kept by children with
asthma. Cats are not a common pet in India. Reports on pets are very
few in this country. If pets are already in the house, contact with the
patient should be minimized; or they should be kept out of the living
premises.
Moulds or indoor fungal spores Prevent seepage of water through roofs or
walls during the rainy season. Keep rooms well ventilated and allow
sunlight in. Children with asthma should not be asked to take out
winter clothing and help in sunning. Similarly they should avoid cleaning
cupboards and drawers which have been closed for some time.

Outdoor Allergens
Seasonal exposure to pollens and fungus can be reduced by keeping the
doors and windows closed from early morning till evening during the
high pollen season. Air conditioning can be used. The filter of the air
conditioner should be properly maintained.
In case an allergen is found to contribute significantly to patient
problem, he should be referred to a specialist for skin testing and if
required, for immunotherapy, only if the child is not responding
appropriately to pharmacotherapy and allergen is significantly
contributing to disease.

Irritants or Chemicals
Avoid tobacco smoke, strong odors, fumes from various kinds of stoves/
chullah and using kerosene, wood or cow dung.

Breastfeeding
In high-risk families (atopy on both sides or even one side) exclusive
breastfeed should continue for 6 months and mother should avoid well
known allergenic foods in diet while the baby is exclusively breastfeed.
Psychosocial Aspects of Asthma Management
Children with chronic illnesses are at an increased risk for developing
psychological disturbances. Children with severe asthma are three times
more likely to develop emotional/behavioural problems as compared to
healthy peers. Mental health workers can provide important services to
asthmatic children who have obvious psychological or behavioural
problems, experience school difficulties and are non compliant with
treatments.
112 Selected Topics in Pediatrics for Practitioners

Family therapy aimed at modifying family interaction problems and

parent child relationships can help in improved management of asthma
and also improve the overall quality of life. Hence, family therapy should
be considered an adjunct to the conventional treatment in severe
asthmatic children. It is important that psychologists be part of the
multidisciplinary team in order to provide comprehensive services to
children with asthma.

AVOIDANCE OF OTHER TRIGGER FACTORS

Viral Infection
At the first sign of cold, short-term treatment with inhaled short acting
β2-agonist maybe instituted. Short-term rescue dose of steroids may be
used, or if child is on inhaled steroids, their dose may be stepped up.

Rhinitis/Sinusitis
In these conditions, the nasal function of warming, filtering and
humidification of air are compromised, they thus act as triggers. Treat-
ment of clinical allergic rhinitis with intranasal sodium chromoglycate
or steroids reduces nasal inflammation, obstruction, postnasal drip and
consequently, symptoms of asthma.

Gastroesophageal Reflux
For children with symptoms suggestive of reflux, and especially those
with nocturnal asthma, avoidance of food and drinks, two hours prior
to bed time, head elevation, thickened foods and treatment with
cisapride/domperidone may be helpful. Oral bronchodilators should be
avoided since these drugs relax gastroesophageal sphincter and may
increase gastric acid section.

Drugs
Drugs like aspirin, NSAIDs, β blockers should be avoided in children
with bronchial asthma.

OTHER TREATMENT MODALITIES

Immuno Therapy
Immuno therapy and immuno modulator drugs have definite evidence
of benefit but find use in a small selected group.
Usage : As an adjunct to pharmacotherapy
Indication : Poorly controlled asthma on optimal pharmacotherapy
in whom allergy testing has shown sensitivity to one or
at the most two unavoidable indoor allergens, e.g. dust
 Current Trends in Diagnosis and Management of Bronchial Asthma 113

mite. Prerequisites, older child > 5 years. Only in a

hospital setting with full resuscitative measures available.
: Experienced personnel
: Asthma relatively stable at time of administration.

Immunosuppressive Drugs
Methotrexate and goldsalt–have the best evidence for positive effects.
Usage : As an adjunct to pharmacotherapy.
Indications : Poorly controlled asthma despite oral steroids + high
dose inhaled steroids with optimal compliance and
elimination of triggers or in whom side effects of oral
steroids are not tolerable.
Pre-requisite : Tertiary care centre/experienced personnel
Yoga : Some qualitative research, performed without controls
has shown beneficial effect. It may be used as a supple-
ment to pharmacotherapy.
 12
Childhood Tuberculosis—
Management Guidelines
MP Jeyapaul

The tubercle bacillus was discovered on March 24th in the year 1882 at
Berlin by Robert Koch. He laid foundation for Mantoux (Mx) test and
BCG vaccination. Incidentally he also died of tuberculosis (TB).

INTRODUCTION
No single country has succeded in the control of TB. In developed
countries also due to emergence of HIV infection, incidence of TB is
increasing. 1/3 of world population is infected with TB. Every year 1
percent of world population is becoming new cases. One infected person
can infect 10 to 15 persons in a year. It causes 6 percent of total deaths
in the world in a year. All the TB deaths are preventable.

Morphology of Mycobacterium Tuberculosis

This is a curved rod in shape, 2 to 4 μ in size, non-motile, non-spore
forming fast pleomorphic, having acid fast character due to the fatty
acids incorporated in the cell wall and an obligatory aerobe. It is slow
growing, and requirer 15 to 32 hours for replication.

Primary Tuberculosis
Usually occurs in children due to first infection.

Reinfection
Reinfection or adult type of tuberculosis occurs at any time after the
primary infection due to endogenous reactivation or exogenous re-
infection. This can occur in pediatric age also. The hall mark of primary
infection is lymphadenopathy, as the primary infection is not limited by
cell mediated immunity. In reinfection, cell mediated immunity helps in
the prevention of spread but at the same time destruction of host tissues
 Childhood Tuberculosis—Management Guidelines 115

occurs causing cavity formation. Healing is by calcification in primary

tuberculosis and in reinfection is by fibrosis. Primary tuberculosis is also
infective but the infectivity is very low because the organisms are not
too many and the child cannot cough with high velocity as in the case
of adults to produce droplet infection.

Primary Complex
The primary focus of tuberculosis infection with the corresponding
lymphadenopathy is called primary complex.

Progressive Primary Complex

Progression of either the primary focus or the progression of the lymph
node swelling causing pressure symptoms on the bronchus resulting in
segmental lesions—either collapse or consolidation or collapse consoli-
dation. With three weeks of broad spectrum antibiotics trial if the lesion
is persistent then the lesions will be called progressive primary complex.

Disseminated Tuberculosis
By lymphatic or hematogenous spread to other systems—abdomen, CNS,
renal, bone, etc. CNS tuberculosis occurs within 2 to 6 months of primary
infection due to this spread. Lymph node and endobronchial TB occurs
with in 3 to 9 months. Bone TB occurs after some years and renal TB
occurs after decades.

Natural Course of Primary Infection

75 to 85 percent outgrow the infection. Only 20 to 25 percent may
develop the disease. During coughing and sneezing the disease spreads
by droplets. First deposition of TB bacilli at the terminal bronchioles
occurs. Bacilli begin to multiply. The alveolar microphages appear within
48 hours. They try to ingest the bacilli. But sulfactides produced by the
bacilli prevent this. Bacilli proliferate within the macrophages and spread
to regional lymph nodes. By this time, T lymphocytes start appearing
and they get activated. They proliferate and produce lymphokines that
activate macrophages to become epithelial cells or multinucleated giant
cells. The activated lymphocytes also produce cytotoxic substances that
causes necrosis or caseation. In HIV infection as T lymphocyte are being
depleted, the activation of macrophages does not occur.

Investigation
Proper history taking and contact tracing are the most important
investigations.
116 Selected Topics in Pediatrics for Practitioners

Mantoux test Intradermal administration of purified protein derivative

of the tubercle bacilli produces delayed hypersensitive reaction if the
child is infected with tuberculosis already. The other important
investigations to prove tuberculosis are identification of the organisms
in the sputum, resting gastric juice or bronchoalveolar lavage by means
of Ziehl-Neelsen staining. In younger children it is difficult to collect the
sputum and also the organisms will not be many in number except in
cavitatory type of tuberculosis. So instead of sputum, resting gastric
juice aspirate is being tested for the organism. After centrifunging the
specimen the deposit will be tested for tubercle bacilli by Ziehl-Neelsen
staining. Previously it was thought that resting gastric juice yields more
positive results than bronchoalveolar lavage. But now as the
bronchoalveolar lavage is being collected at the site or close to the
lesion, bronchoalveolar lavage yields more positive results. The macrospic
appearance, biochemical characteristics and Ziehl-Neelsen staining of
the pleural aspirate, CSF or aspirate from the lymph nodes will help in
the diagnosis. Fine needle aspiration is slowly replacing the biopsy.
Culture of the tubercle bacilli Takes at least 6 to 8 weeks as the growth of
tubercle bacilli is slow. Culture medium used is Lowenstein-Jensen—
egg based medium.
Bactec system Here the fatty acid subtracts like palmitic acid and formic
acid labeled with radioactive carbon is used as the medium. When
mycobacteria metabolise the fatty acids, the radioactive CO2 is released
and is measured as a marker of bacterial growth. Here the culture report
can be got in a week.
Radiology The findings from chest X-ray such as patchy pneumonitis,
hilar nodes, presistent collapse, collapse consolidation are not the proofs
for tuberculosis. We have to look for the other evidences as either positive
Mx or positive contact history or other corroborative evidence to confirm
the diagnosis.
CT scan is helpful in the dignosis of neurotuberculosis—Tuberculoma
and TB meningitis.
USG findings will be more helpful in diagnosing abdominal tuberculosis.
Thickened omentum, enlarged mesenteric lymph nodes, thickened
intestinal walls and the presence of adhesions will more or less confirm
the diagnosis. But still the gold standard is laparoscopic biopsy.
Serological tests Serological data will tell about the humoral immune
status comparable to Mx test that tells about cell mediated immunity.
IgM antibodies rise with primary infection and IgG antibodies rise when
infection becomes established. This test has its own limitations as it
 Childhood Tuberculosis—Management Guidelines 117

becomes positive with other mycobacterial infections and prior BCG

vaccination also will influence the results. It cannot differentiate whether
this is an infection or disease and also whether this is an active disease
or healed disease.
Nucleic acid amplification PCR will be able to detect even a single
mycobacterium present in the sample by detecting the DNA or RNA
material of tuberculosis in the given specimen. High false positivity due
to contamination, high cost, the necessity of a big lab back up are the
limiting factors.
Through sophisticated tests like, PCR, bactec and serological tests are
available, still we have to depend on the time tested and conventional
aids such as proper elicitation of contact history, Mx test, chest X-ray
and clinical findings to confirm the diagnosis.

MANAGEMENT

First line drugs Second line drugs

H-Isoniazid—1952 Amikacin
R-Rifampicin—1962 Ciprofloxacin
S-Streptomycin—1947 Ofloxacin
Z-Pyrazinamide—1952
E-Ethambutol—1961

Thiacetazone and PAS are withdrawn drugs now. Streptomycin is

used only in resistant TB.
Isoniazid It inhibits the synthesis of mycolic acid which is the unique
component of mycobacterial cell wall. It is a hepatotoxic drug as it is
metabolised in the liver. Dose is 5 mg per kg. Clinical manifestation of
pyridoxin deficiency in children due to INH is rare. So B6 replacement
with vitamin B6 is not essential.
Rifampicin Dose is 10 mg per kg. It is to be given in empty stomach
as absorption is well during fasting. It is a hepatotoxic drug. Always
INH and rifampicin are combined to prevent drug resistance to develop
to either one of the drugs. It kills mainly persisting bacilli inside the cell.
So rifampicin is called a sterilizing drug.
Side effects Orange discolouration of urine occurs. Allergic rashes can
occur.
Pyrazinamide The dose is 25 mg per kg. In all the regimens this is given
only for 2 months as resistance to this drug develops quickly. It is more
effective in acidic medium. So the organism in the caseous material are
taken care of by pyrazinamide. So it is also a sterilizing drug.
118 Selected Topics in Pediatrics for Practitioners

INH, rifampicin and pyrazinamide are all hepatotoxic drugs. When

SGPT level increases to three times normal, all the three hepatotoxic
drugs are to be stopped. The non-hepatotoxic drugs such as ethambutol
and streptomycin are to be continued till SGPT level comes to normal.
After that the hepatotoxic drugs can be restarted one by one.
Ethambutol Dose is 15 mg per kg. The purpose to add ethambutol is
to prevent emergence of resistance to other TB drugs. Optic neuritis is
the complication but is reversible on stopping the drug.
Streptomycin Dose is 15 mg per kg. Toxic to vestibular and auditory
portions of VIII cranial nerve. If it is given to antenatal mother then off
spring may be born deaf.
Second line of drugs Commonly used second line drugs in resistant TB
are ciprofloxacin and ofloxacin. Though theoretically both may cause
destruction of growing cartilage, in actual practise this side effect is rare.
Indian Academy of Pediatrics has worked out a consensus statement
on the management of childhood tuberculosis. Which will severe as a
ready reckoner for all practicising physicians.

Treatment of
Childhood Tuberculosis—
Consensus Statement
A Parthasarathy

After long deliberations in 1997 the IAP Working Group on Management of

Childhood Tuberculosis came out with consensus statement. The same has been
reproduced below to benefit the practitioners.
In order to optimize treatment protocol, tuberculosis has been classi-
fied into five groups based on clinical types. Suggested regimen for
drug therapy in each of these groups is as follows:
 Childhood Tuberculosis—Management Guidelines 119

Group I
Preventive therapy Drug Regimen
1. Asymtomatic mantoux Mx +ve < 3 years

}
2. Asymptomatic Mx +ve < 5 years with
grade III or IV PEM
3. Mx +ve—Recent Converter/no signs - 6 HR
Healed lesion—Normal chest X-ray or
calcification/ fibrosis
4. Children < 3 years with H/O + ve contact
5. Children < 5 years—grade III or IV PEM with
H/O + ve contact as defined—below
Group 2

}
1. Primary complex (lungs)
2. Symptomatic Mx + ve < 3 years—
without localization
3. Symptomatic Mx + ve < 5 years
with grade III or IV PEM 2 HRZ/4 HR
without localization
4. Isolated lymphadenitis
5. Pleural effusion
Group 3

}
• Progressive pulmonary disease
• TB Lymphadenitis—multiple 2 HRZE/4 HR
• (In case of non-resolution of lesion, extend
continuation phase by 3 months)

Group 4

}
• Miliary/disseminated disease
• Cavitatory disease/bronchopneumonia 2 HRZE/7HR
• Osteoarticular disease
• Abdominal, pericardial, genitourinary TB

Group 5
Neurotuberculosis } 2 HRZE/10 HR
120 Selected Topics in Pediatrics for Practitioners

Dosage recommendations

Daily therapy mg/kg Intermittent therapy mg/kg

+
INH 5 15
RMP 10 15
PZA 25 30*
EMB 20 30*
SM 20 30*
Prednisolone 1 –

+ Never < 5 mg/kg; to be rounded off to the closest higher doses

* No studies conducted in children.

Comments All the drugs should be administered in a single daily dose

on an empty stomach. The drugs are safe, if used in recommended
dosage schedule. Vitamin B6 is not necessary for children taking INH.
Hepatotoxicity may be seen in vulnerable patients (PEM/Disseminated
disease).

Daily vs intermittent therapy A daily treatment regimen is advised.

Intermittent therapy regimen is not recommended as compliance is
generally poor and there is an increased risk of drug resistance. However,
it may be considered only if compliance is assured.

Single drug or fixed-drug combinations Fixed-drug combination of

INH and RMP is acceptable. It is ideal to use PZA separately.# Pharmaco-
kinetic data regarding triple fixed dose combination in children is not
adequate. Change in prescription from triple fixed dose combination to
double fixed dose combination after first two months of treatment, may
be confusing to the patient.

Prednisolone
Indications
• Neuro-TB/miliary TB 1 mg/kg/day
• TB involving serous layers for 4-8 weeks
• Endobronchial TB/segmental lesions Neuro-TB (8-12 weeks)
• Genitourinary TB/sinus formation

Special Conditions
• Pregnancy: 9 HRE (SM and PZA are contraindicated)
• In case of neuro-TB, PZA may be used 2 HRZE/7 HR
 Childhood Tuberculosis—Management Guidelines 121

Baby Born to Mother with TB

(Diagnosed in 3rd Trimester or During Delivery)
• Breastfeeding must be continued
• BCG vaccine should be given at birth
• If chest X-ray is normal, then 6 HR
• If chest X-ray is abnormal, then 2 HRZ/7 HR
• Congenital Tuberculosis: 2 HRZ/7 HR
Hepatotoxicity Clinical symptoms, hepatomegaly and jaundice merit
laboratory tests and temporary stoppage of hepatotoxic drugs (HRZ).
Routine monitoring of SGPT is not recommended.

Suggested Actions
• Stop INH, RMP and PZA
• Start SM and EMB
• When SGPT returns to near normal (usually 2-4 weeks), Restart INH
at 5 mg/kg. Continue SM and EMB. Restart RMP after 1 week
• Stop SM and EMB
• Restart PZA after 1 week (If stoppage occurred in intensive phase of
therapy).
Defaulters Defaulter treatment discontinued for > 1 week against medical
advice. Lost to treatment period of default > 1 month.
Suggested actions Default period between 1 week to 1 month – continue
the same phase of treatment for an additional 1 month. If default period
is > 1 month, restart full treatment.
Drug resistance If a patient on prescribed treatment does not respond,
check drug compliance, confirm diagnosis and assess for probable adult
contact with multidrug resistant TB. Arrange for bacteriological study,
if possible. A child with cavitatory disease or history of past treatment
for TB is vulnerable.In case of suspected drug resistance in absence of
bacteriological proof, suggested drug regimen – 2 SHRZE/1 HRZE/ 6
HRE.
In case of proved drug resistance, suggested drug regimen is as
follows.
Drug Resistance

HIV status INH RMP Multidrug

HIV –ve 12 RZE 18 to 24 HZE 3 sensitive drugs for

2 years after culture -ve
HIV +ve 18 RZE or 12 months 18 to 24 or 12 months 3 sensitive drugs for
after culture -ve after culture -ve 2 years after culture -ve
122 Selected Topics in Pediatrics for Practitioners

Relapse definition Reappearance of signs and symptoms of tuberculous

disease within 2 years of cure after completion of specified therapy.
Relapses are rare in children.
Suggested drug regimen Treat as suspected drug resistance in the absence
bacteriological proof.
Contact definition Any child who lives in a household with an adult
taking ATT or has taken ATT in the past 2 years.
Indications of preventive therapy for contacts < 3 years/ < 5 years with PEM
grade III and IV/adolescents. Close surveillance is necessary for 5 to 12
years old contacts. Suggested preventive therapy for contacts: 6 HR.
BCG adenitis If lymph node is small (< 1.5 cm), no treatment is required.
Increasing size or fluctuant—excision or 3 to 6 H Sinus formation:
Excision.

BIBLIOGRAPHY
1. Udani PM. Tuberculosis in Children. In: IAP Textbook Pediatrics (2nd edn):
Parthasarathy A, Menon PSN, Nair MKC (Eds). Jaypee Brothers Medical
Publishers: New Delhi, 2002;212-14.
 13
Management of Acute Diarrhea
VS Sankaranarayanan, S Srinivas

INTRODUCTION
Acute diarrheal disease is one of the major killers in children of the
developing countries. High mortality in acute diarrhea is attributed to
loss of water and electrolytes, leading to dehydration which may be so
severe as in cholera and other acute secretary diarrhea with large purge
volume and rate that it may prove fatal if not managed early. Repeated
and prolonged episodes of diarrhoea can result in malnutrition—diarrhea
malnutrition cycle resulting in high mortality. A management protocol
for acute diarrhoea consisting of “Triple A” approach has been found to
be rewarding in our set up and hence recommended.

What is ‘Triple A’ Approach?

It consists of assessment, analysis of clinical presentations and action
plan protocol for acute diarrhoeal diseases.

What to Assess?1,2
1. Status of hydration (No dehydration, some dehydration (5-10%) or
severe dehydration (> 10%).
Note: Thirst and irritability with reduced and dark coloured urination
are the earliest features of dehydration.
2. Status of nutrition of the child (any malnutrition?).
3. Any co-morbid extra gut infections (like wheezy LRI, pneumonia,
septic tonsillitis, UTI, septicemia, etc.).
4. Any prior treatment details? (any abuse of drugs like empirical
antimicrobes , WHO banned drugs, prolonged use of low calorie and
only starchy feeds, failure of breastfeeding, use of unclean feeding
bottles, lack of hand washing techniques, etc.).

What to Analyse in a Given Patient of Diarrhea?

Categorical clinical pattern of presentation of diarrhea:
a. Acute watery diarrhoea (infective origin within two weeks of
presentation).
124 Selected Topics in Pediatrics for Practitioners

b. Acute dysentery (history of passage of blood and mucus per rectum

within two weeks of presentation).
c. Persistent diarrhoea (onset as acute watery diarrhoea persisting over
two weeks without improvement due to infective cause).
d. Chronic diarrhoea (often over four weeks due to noninfective cause,
not warranting any antimicrobes, e.g. malabsorption syndrome, small
bowel mucosal disease, cow’s milk protein allergy, etc.).
In acute watery diarrhea (AWD), especially of prolonged duration,
i.e. > 1 week, it is desirable to make sure whether the diarrhoea is
secretory or osmotic or invasive nature of presentation.
Secretory diarrhea is often large volume, watery, presents even during
bowel rest and is unrelated to feeds, whereas osmotic diarrhoea is often
small and watery, precipitated by offending feeds and relieved by non-
offending feeds (e.g. milk feeds) due to injury to brush border and
epithelial cell with reduced disaccharidase activity.
Invasive diarrhoea presents as dysentery with blood and mucus in
stools often due to infective cause, e.g. EIEC, EHEC or Entamoeba
histolytica causing inflammation of large bowel. In bacterial colitis, the
stool is small, more frequent with blood and mucus with no faecal
matter with constitutional symptoms like fever, toxemia, abdominal
pain and tenesmus in young infants (< 2 years) when compared to
mixture of blood, mucus and faces with less constitutional symptoms in
over 2 years of children in protozoal amoebic colitis. Stool microscopy
is confirmatory which shows sheets of pus cells and RBCs in bacterial
colitis and more RBCs and less leukocytes with EH trophozoites in
amoebic colitis.
Management Protocol of AWD/Dysentery (Action Plan)

Plan A Plan B Plan C

No dehydration Some dehydration Severe dehydration

Objective Prevention of Correction of Correction of severe
dehydration, mild-moderate dehydration and
malnutrition ORS dehydration by electrolyte imbalance
optional ORS and shock by IVF
Where Home ORT corner Intensive care
By whom Mother/caretaker Under supervision Doctor and staff
in a health facility

Antimicrobes for Specific Cause in Acute Diarrhea

Cause Drug of choice Dose

Cholera Tetracycline 30 mg/kg/day qid × 3 days 6 mg/kg d bd × 3 days

Doxycycline 5 mg/kg qid × 3 days
Furazolidone

Contd...
 Management of Acute Diarrhea 125

Contd...

Cause Drug of choice Dose

Dysentery TMP + SM TMP 5 mg/kg + SM 25 mg/kg

Bd × 5 days
NDA 15 mg/kg/qid × 5 days
Ampicillin 25 mg/kg/day tid × 5-10 days
Quinolones 10-15 mg/kg/day bd × 5 days
Amoebiasis Metronidazole 30 mg/kg/day tid × 5-10 days
Giardiasis Metronidazole 15 mg/kg/day tid × 5 days
Tinidazole 10-15 mg/kg/day tid × 5 days

Note: Treat extra gut infections appropriately.

Composition (gm/L) and Concentration (mmol/L) of ORS

WHO ORS Low osmolar ORS

Sodium chloride (gm/L) 3.5 2.6

(mmol/L) Na-90 Na -75
Cl-80 Cl -65
Pottasium chloride (gm/L) 1.5 1.5
(mmol/L) K+ -20 K+ - 20

Trisodium citrate (gm/L) 2.9 2.9

(mmol/L) Citrate-10 Citrate-10
Glucose anhydrous (gm/L) 20 13.5
(mmol/L) Glucose-111 Glucose-75
Water 1 litre 1 litre
Total Osmolarity 311 245
Recommendation Cholera Noncholera diarrhea and neonatal
diarrhea

Dose of ORS for Some Dehydration when Body Weight is not Known

Age ORS (ml) Glass

< 4 months 200-400 1-2

4-11 months 400-600 2-3
12-23 months 600-800 3-4
2-4 years 800-1200 4-6
5-14 years 1200-2200 6-11
> 15 years > 2200 12-20

Encourage breastfeeding. If not breastfed give extra 100-200 ml of

water (< 6 month).

Maintenance Dose of ORS

• 50-100 ml/kg in 24 hours in between feeds or
• 50-200 ml of ORS after each loose stool to prevent dehydration till
stools get olidified for non-dehydrated patients ORS is only optional.
126 Selected Topics in Pediatrics for Practitioners

Few Guidelines of ORS Administration

Hand on training for mixing ORS to the mothers
• Use only local measures like tumblers and cups
1-2 teaspoonful frequently for less than 2 years and frequent sips
from a cup for older children
• If the child vomits wait for 10 minutes and then try a teaspoonful of
ORS frequently
• Educate mothers for danger signs.

WHO ORS in Severely Malnourished4

Hospitalise the Patient
• Slow and prolonged rehydration with low sodium ORS over 12-24
hours of 70-100 m/kg body weight
• Watch for signs of fluid overload
• Once hydrated give 5-10 ml/kg of WHO ORS for every loose stool
• Plain water allowed ad-lib. Initially parenteral fluid therapy preferred
mostly
• Promptly treat hypoglycemia/hypo-potassemia/hypothermia and
infection
• Start enteral feeding at the earliest with supplemental potassium
with food for two weeks

Contraindications for Use of ORS

• Persistent vomiting
• Dehydration worsening (no improvement within 8 hours)
• Severe dehydration
• Refusal of ORS
• Neonates and severely malnourished infants
• Complications like abdominal distension, respiratory distress,
convulsions and anuria
• Rarely glucose malabsorption

New Improved ORS Formulations

Cereal based ORS (Rice based ORS)3
50 gm of cooked/pop rice powder replaces 20 gm of glucose in ORS

Advantages
Home available, acceptable and cheap low osmolarity—slow release of
glucose with no risk of osmotic diarrhea.
 Management of Acute Diarrhea 127

Additional peptides and amino acids for absorption/calorie superior

to WHO ORS.

Disadvantages
• Low bedside life—8-10 hours
• Time consumed for prior cooking
• Incomplete digestion of starch < 3 months of age ?
• Poor compliance with commercial rice based ORS

Low Osmolar ORS5

Advantages of Low Sodium ORS
• Management of non-choleric diarrhoeal dehydration
• Newborns and infants
• Prevention of dehydration
• During maintenance of hydration
• Malnourished young infant
• Low osmolarity
• Replaces exact loss, efficacious.

Citrate based ORS

Currently recommended by WHO to replace bicarbonate.

Advantages
• Increased shelf life
• Improved taste
• Cheaper
• Na+ absorption in high output diarrhoea
• No soiling of packets 2.9 gm/L of sodium citrate will give a concen-
tration of 10 mEq/L of citrate.

Super ORS 1984 (Patra Mahalanabis et al).

Glucose glycine based ORS was called the super ORS because it was
thought to cause:
• Reduction in stool volume 50%
• Reduction of ORS requirement 43%
• Reduction in duration of diarrhea 40%
It was disproved by subsequent studies. The current concept is that
glycine based WHO ORS is safe and effective but cost prohibitive.
128 Selected Topics in Pediatrics for Practitioners

Severe Dehydration—Parenteral Fluid Therapy

Age 30 ml/kg in Then give 70 ml/kg in Total 100 ml/kg in
Infants one hour next five hours six hours
Older half hour next 2 and a half hours three hours
Children
Note: IV fluid of choice is 5% D in ringer lactate

IVF Therapy in AWD in Severely Malnourished Infant

Fluid volume: 75-100 ml/kg over 10-12 hours
IVF 0-2 hours 2-12 hours
RL + 5% GDW or
0.45% N/S + 5% GDW or 15 ml/kg 5-7 ml/kg/hours
0.45% N/S made in
bicarb +5% GDW
If no improvement, blood/plasma 10 ml/kg over 3 hours
If in septic shock, maintain temp + colloids in addition
If hypoglycemic, 1 ml/kg of 50% glucose bolus

WHO Banned Drugs and Drugs not Recommended

1. Neomycin
2. Stool binders like kaolin and pectin
3. Anti motility drugs like loperamide
4. Opiates and steroids
Drugs not recommended include
Antiemetics and empirical anti microbes as a routine.

Adjunct Therapy in Acute Diarrhea

1. Zinc Supplementation: Zinc supplementation in AWD is
recommended especially in developing countries as the children with
malnutrition and subclinical zinc deficiency will be benefited. Zinc
supplementation has beneficial effect on diarrhoea by reducing stool
frequency and duration.6 Zinc plays a vital role in electrolyte transport
 Management of Acute Diarrhea 129

crypt cell regeneration and early repair of mucosal damage, synthesis

of digestive enzymes which reduce osmotic diarrhoea and improve
immunity.7
2. Vitamin A supplementation. It needs to be known that even in the
presence of diarrhoea, vitamin A is satisfactorily absorbed from the
intestine. Vitamin A supplementation is recommended, especially in
severely malnourished children with diarrhoea who have not received
it earlier during the six months in a dose of 200,000 IU if > 10 kg and
100,000 IU in children < 10 kg. Vitamin A supplementation results
in the reduction of overall childhood mortality by maintaining
integrity of both GI tract and respiratory tract epithelium and vitamin
A deficiency alters the mucosa susceptible for bacterial infection.8
3. Probiotics and prebiotics in diarrhea prebiotics are viable microbial
food supplements which beneficially influence the health of humans.9
Prebiotic is a non-digestible ingredient stimulating the growth and
or activity of probiotic strains of bacteria in the colon and thus benefits
health of the host. Probiotics are lactobacilli, Bifidobacterium bifidum,
streptococcus thermophilus and Sacharomyces boulardii in the form of
fermented foods like curd, yoghurt.

Characteristics of Probiotics
1. Maintenance of microbial mines to the hosts advantage
2. Decrease fold of pathogenic bacteria
3. Resistent to gastric acid, bile and digestion
4. Have ability to adhere to and colonise the gut
Mechanism of action of probiotics11 are competing for nutrients,
competing for receptor (adhesion) sites, acidification, production of
inhibitory substances (bacteriocins) and immunomodulation
(increases IgA levels) studies reveal some probiotics can significantly
shorten the duration of rotavirus and other acute diarrhoea.10
We feel that it is needed in persistent diarrhoea and in mal-
nourished diarrhoeal children.
Dose of Probiotics

Probiotic Dose How long?

Lactobicillus acidophilus 108 organisms/G of probiotic 3 days

supplement bid

Lactobacillus+streptococcus tid between meals 5 days

Faecalis + clostridium butricum +
Bacillus mesentericus (symbiotic) 1

Sacharomyces boulardii 282.5 mg/sachet bid 5 days

130 Selected Topics in Pediatrics for Practitioners

5. Racecadotril. It is an encephalinase inhibitor, which reduces intestinal

hypersecretion in both animals and human beings but does not
decrease motility. Studies concluded that Racecadotril is safe and
well tolerated in acute watery diarrhoea in a dose of 1.5 mg/kg body
weight orally every 8 hours.12
6. Bismuth subsalicylate One of the oldest proprietary preparation,
commonly used to treat diarrhoea in USA for more than 75 years.
Studies reveal that Bismuth subsalicylate, when used as an adjunct
to oral rehydration effectively shortens the period of acute watery
diarrhoea in infants and young children in a daily dose of 100 or 150
mg/kg orally.13
Feeding during acute diarrhea Based on child’s age, pre illness feeding
pattern and hydration status.14

During rehydration After hydration

Breastfed infants Continue breastfeed Breastfeed frequently

Non-breastfed ORS (0-4 hrs) Add home available Home available
infants feeds with salt feeds
Severely Early home available energy rich 4-6 months of age. Breast-
malnourished hypoallergenic feeds with low osmolar feed + energy rich weaning
ORS feds. Energy rich hypo-
allergenic frequent feeds

REFERENCES
1. Patwari AK. Management of acute diarrhoea in children, Pediatrics for you-
Yearbook. Vol III, 1997;15-28.
2. Indian Academy of Pediatrics, Guidelines for management of diarrhoea in
Children – Report of IAP Task Force on Diarrheal Diseases 1991.
3. Bhan MK, Mahalanabis D, Fontaine O, Pierce NF. Clinical trials of improved
oral rehydration salt formulations. A review, WHO Bulletein 1994;72: 945-55.
4. Nagpaul A, Aneja S, Oral rehydration therapy in severely malnourished children
with diarrhoeal diseases. Indian J Paediatr 1992;59:313-19.
5. International study group of reduced osmolarity ORS solutions. Multicentre
evaluation of reduced osmolarity oral rehydration salts solution. Lancet
1995;345:282-85.
6. Sazawal S, Black RE, Bhan MK et al. Zinc supplementation in young children
with acute diarrhoea in India. New Engl J Med 1995;333:839-44.
7. Dutta P: Zinc and diarrhoea. The Child 1994;3:81-84.
8. Dutta P. Acute diarrhoea of recent advances in pediatrics Special Vol 6
Gastroenterology, Hepatology and Nutrition by Suraj Gupte 2000;7:70-92.
9. Salminen S, Human studies on probiotics: Aspects of scientific documentation.
Scand J Clin Nutr 2001;45(1):8-12.
10. Pant A R et al. Lactobacillus GG and acute diarrhoea in young children in the
tropics. J Trop Pediatrics 1996;42:162-65.
11. Salminen S, Isolauri E, Salminen E. Clinical uses of probiotics for stabilizing
the gut mucosal barrier: Successful strains and future challenges. Asia Pacific
J Clin Nutrition 1996a;5:53-56.
 Management of Acute Diarrhea 131

12. Salazar-LindoE, Santisteban-Ponce J Cheawoo E et al. (Hosp. Nacional cayetano

heredia, lima, peru), Racecadotril in the treatment of acute watery diarrhoea.
N Engl J Med 2000;343:463-67.
13. Figueroa-Quintarilla D, Salaza-Lindo E, Sack RB, Leon Barua R, Sarabia-Arce
S, Campos-Sanchez M. Eyzaguirre-Maccane (instituto national de salud del
nino, lima, peru. Universsial peruana cayetano heredia. Lima: Johus Hopkins
univ. Baltimore MD. A controlled trial of bismuth subsalicylate in infants with
acute watery diarrhoeal disease. N Engl J Med 1993;328:1653-58.
14. Jelliffe DB, Jelliffe EFP. Dietary management of young children with acute
diarrhoea (2nd edn), WHO: Geneva1991;3-26.
 14
Neonatal Cholestasis
Syndrome Practical Approach
BR Thapa

Introduction
Neonatal cholestasis is a pathological condition in which bile flow is
affected. Neonatal cholestasis syndrome (NCS) comprises of hetero-
geneous group of hepatobiliary disorders responsible for cholestasis
during neonatal life. The cholestasis due to some disorders can extend
beyond neonatal period hence; this is appropriate to call this syndrome
as cholestasis of infancy. Most of the disorders have linkage with insults
during antenatal, natal and postnatal periods indicating intrauterine or
postnatal events. Main causes of NCS are infections, metabolic disorders
and extrahepatic biliary obstructions.1

Epidemiology
The present scenario about the spectrum of illnesses is changing fast, the
premature babies are now being looked after in neonatal specialized
care units, the causes of cholestasis due to sepsis, total parenteral nutrition
(TPN), drugs, etc. are emerging as another large group. But this remains
a challenge to evaluate and manage NCS because of fast change in the
diagnostic and therapeutic approach world over. It becomes mandatory
to define the cause of NCS that needs battery of tests to carry out. This
is also important to do various tests simultaneously to differentiate
between neonatal hepatitis (NH) and extra hepatic biliary atresia (EHBA)
to avoid delay in surgical treatment of EHBA.2

Approach to Jaundice
Jaundice is a very common symptom encountered during neonatal life.
Approach to jaundice during neonatal period and infancy is given Figure
14.1. This is also called hyperbilirubinemia when defined by raised
serum bilirubin > 2 mg/dl. Based upon the composition of serum biliru-
bin, this is divided into unconjugated and conjugated hyperbilirubinemia.
Unconjugated hyperbilirubinemia a very common during first few weeks
 Neonatal Cholestasis Syndrome Practical Approach 133

of life and the unconjugated bilirubin constitutes 80 percent of total

serum bilirubin level. This is characterized by icterus, normal colored
urine and yellow normal colored stools. Most of the times it is attributed
to physiological jaundice or breast milk jaundice.

Definition
Conjugated hyperbilirubinemia is defined when the conjugated fraction
of bilirubin is more than 20 percent of the total serum bilrubin or when
conjugated bilirubin more than 1.5mg/dl in neonatal period and persist
beyond first 14 days of life then it is labeled as neonatal cholestasis.This
is associated with retention of bile salts in the blood. Cholestasis is also
defined as pathological stage of reduced bile formation or flow and
clinical criteria are passage of high colored urine that stains the diaper
yellow and pale/white/acholic or intermittent pale and yellow or yellow
stools. Cholestasis is characterized by itching that may not be recognized
during early life but irritability is a common feature. After 6 months of
life itching is quite apparent. These clinical pointers are very important
to differentiate between cholestasis and unconjugated hyper-
bilirubinemia. Histopathological definition of cholestasis is the appear-
ance of bile within the liver parenchyma responsible for secondary cell
injury.

Classification
It is important to divide neonatal cholestasis into 2 groups, which are
well defined now, and are intrahepatic cholestasis and extrahepatic
cholestasis (Fig. 14.1) based upon the nature and site of pathological
lesions. Intrahepatic cholestasis covers two important groups
hepatocellular cholestasis: Neonatal hepatitis and paucity of intrahepatic
bile ducts (PIBD). For better understanding cholestasis can also be
classified into neonatal hepatitis and obstructive cholaniopathy or
obstructive cholestasis. Obstruction could be at level of extrahepatic
biliary tree and or intrahepatic biliary tree also called PIBD.2,3

Factors Predisposing
Newborn infants are more prone to develop cholestasis because of
immaturity of excretory function, inborn errors of metabolism manifesting
in early life and inherent susceptibility to various viral, septic and toxic
insults. The immature liver cells are associated with peculiar kind of
pathological response to different kind of noxious agents during neonatal
life and infancy.
The ineffective enterohepatic circulation of bile further compromises
the excretory function. There is gradual maturation of hepatocytes in
134 Selected Topics in Pediatrics for Practitioners

Jaundice

Hyperbilirubinemia
(S. Bilirubin > 2 mg/dl)

Conjugated Unconjugated
• S. Bilirubin > 20% • S. bilirubin. 80%
• Urine high colored • Urine color normal
• Diaper staining • Stool color normal
• Stool clay or normal colored

Cholestasis

Intrahepatic Extrahepatic
• Clay or normal • Clay colored stools or
colored stools interm ittent

• Neonatal hepatitis • EHBA

• PIBD • Choledochal cyst
• Others correctable

Fig. 14.1: Approach to jaundice during infancy and classification of cholestasis

respect to handling of bilirubin, excretion of bile, synthetic functions

and enzyme system during infancy. The maturation of these functions
may be equivalent to adulthood by age of 4-6 months. Some biochemical
markers of cholestasis like alkaline phosphates and glutamyl
transpeptidase are raised during early life. Serum unconjugated bilirubin,
and bile acids concentration are normally in higher concentration in
blood again suggesting that there are clearance problems in neonatal
liver. Due to these reasons the neonatal hepatobiliary system is affected
by various infective, metabolic and obstructive cause faster as compared
to older children and adults.2

Etiology
Various causes of cholestasis1-3 are given in Table 14.1. The spectrum of
cholestasis of infancy seen in our center is like this: Neonatal hepatitis
62 percent extrahepatic biliary atresia (EHBA) 30 percent,choledochal
cyst 6 percent and PIBD 2 percent, Etiology of neonatal hepatitis is as
idiopathic neonatal hepatitis in 54 percent, bacterial infection 18.5 percent,
intrauterine infection 8.5 percent, metabolic disorders 8.5 percent and
miscellaneous 10 percent.4,5
 Neonatal Cholestasis Syndrome Practical Approach 135

Pathophysiology
The effects of cholestasis are devastating secondarily due to retention of
bile and results into widespread problems with the advancing life, of
the cholestatic infants and children. Figure 14.2 gives the consequences
of prolonged cholestasis.

Fig. 14.2: Consequences of prolonged cholestasis

Table 14.1: Causes of cholestasis in infancy

A. Extrahepatic
Correctable
• Biliary atresia • CBD ligation
Non-correctable
• Bile duct stenosis • CBD stricture
• Spontaneous perforation of bile duct • Biliary hypoplasia
• Common bile duct (CBD) stone • Pancreatico-ductal anomaly
• Primary sclerosing cholangitis (PSC) • Choledochal cyst
• Mass (neoplasia)

B. Intrahepatic
I. Idiopathic neonatal hepatitis
II. Intrahepatic cholestasis: persistent
a. Nonsyndromic PIBD
b. Syndromic PIBD

Contd...
136 Selected Topics in Pediatrics for Practitioners

Contd...

c. Others
• Arteriohepatic dysplasia (alagille syndrome)
• Progressive familial intrahepatic cholestasis (PFICI, II, III and IV)
• Byler disease (PFICI)
• Trihydroxycoprostanic academia
• Zellweger syndrome (cerebrohepatorenal syndrome)
III. Intrahepatic cholestasis: recurrent
a. Familial benign recurrent cholestasis
b. Hereditary cholestasis with lymphedema
c. Alpha 1 antitrypsin deficiency
d. Miscellaneous
• Cystic fibrosis
• Idiopathic hypopituitarism
• Hypothyroidism
• Multiple acyl-CoA dehydrogenation deficiency
IV. Hepatitis
a. Infections
• Bacterial infections • Malaria
• Hepatitis B virus • Toxoplasmosis
• Herpesvirus • Tuberculosis
• Coxsackievirus • Syphilis
• Cytomegalo virus • Listeriosis
• ECHO virus
• Rubella virus
• HIV
• Varicella virus
b. Metabolic disorders
A. Disorders of amino acid metabolism
• Tyrosinemia
• Hypermethioninemia
B. Disorders of lipid metabolism
• Colestasis associated with parenteral nutrition
• Niemann-Pick disease type C
• Infantile Gaucher disease
C. Disorder of carbohydrate metabolism
• Galactosemia
• Fructosemia
• Glycogen storage disease, III and IV
V. Genetic chromosomal disorders
• Trisomy F
• Down syndrome
• Donohue syndrome (leprechaunism)
VI. Miscellaneous
• Histocytosis X
• Congenital hepatic fibrosis
• Shock
• Caroli’s disease
• Intestinal obstruction
• Indian childhood cirrhosis(ICC)
• Neonatal iron storage disease/hemochromatosis
 Neonatal Cholestasis Syndrome Practical Approach 137

Approach to NCS
In NCS it is mandatory to differentiate between neonatal hepatitis and
EHBA. Neonatal hepatitis warrants medical treatment whereas
obstructive cholestasis largely EHBA needs only surgical treatment and
is effective, done within 60 days of life.
If the baby is passing pale or acholic or white stools form very
beginning or starts after few weeks of life one should act very fast to
make the diagnosis of EHBA. There is no point in wasting time. In
EHBA fibrosis sets in as early as 4 weeks of life. EHBA babies are usually
term born and have good weight. Twenty percent of these babies may
have associated congenital malformations. Liver function tests at times
may not help to differentiate. Liver enzymes like ALT and AST are
nearly normal in EHBA but are always raised in NH. GammaGT may
be raised in EHBA. In EHBA prolonged PTI usually responds to vitamin
K administration.
The approach to cholestasis to differentiate between obstructive
cholestasis and hepatocellular cholestasis is given in Figure 14.3 whereas
approach in late presentation of EHBA is given in Figure 14.4.

Fig. 14.3: Algorithmic approach to differentiate EBHA from NH (< 60 day)

138 Selected Topics in Pediatrics for Practitioners

Fig. 14.4: Approach to late presentation of EBHA > 60 day of life

Ultrasound
Ultrasound is a non-invasive modality to see the status of liver
parenchyma, dilated intrahepatic or extrahepatic biliary tree and presence
of gallbladder. Conditions like choledochal cyst, bile plug syndrome,
common bile duct(CBD) stone and Caroli’s disease can be picked up
with great accuracy. Absence of gallbladder people have correlated with
EHBA with low sensitivity and specificity (60-70%). But there is significant
overlap. Even in severe cholestasis gallbladder may not be defined
because of less production of bile and it may be hypoplastic.
Ultrasonographic triangular cord (TC) sign is a cone shaped fibrotic
mass infant of bifurcation of portal vein. This is very specific for EHBA
in expert hands7.

Scintigraphy (HIDA Scan)

In severe cholestasis due to NH there may not be excretion of dye even
after adequate priming with phenobarbitone for 5 days 5 mg/kg/day
or ursodeoxycholic acid (UDCA) 2 mg/kg/day. However, EHBA or is
ruled out where dye is seen in duodenum. The sensitivity is very high
to pick up severe cholestasis whereas specificity to pick up EHBA is
very low 60-70 percent. In some centers this investigation is not done
routinely since there is wastage of 6-7 days period.
 Neonatal Cholestasis Syndrome Practical Approach 139

Liver Biopsy
This is important to do liver biopsy. But for interpretation, there is need
of an expert pathologist who is familiar with developing neonatal liver
and then reaction to various toxic factors like infections, metabolic and
obstructive insults. In best hands histopathology can differentiate NH
and EHBA up to the tune of 95 percent. But in 5 percent cases there can
be overlap problems to label.4

EHBA
EHBA is characterized by presence of proliferation of interlobular ducts,
plugged with bile casts and portal tracts show fibrosis. The liver
parenchyma may be normal however, may show intrahepatocytic or
canalicular cholestasis. But in advanced cases after 2 months of life there
may be full-fledged changes of secondary cirrhosis.

Neonatal Hepatitis
In neonatal hepatitis there is marked parenchymal injury suggesting
focal necrosis, ballooning degeneration, gaint cell transformation,
inflammatory infiltrate, pseudoacinar formation and portal tract may
show mild portal triaditis. There is no fibrosis until the disease is chronic.
Metabolic liver disease can be diagnosed.

PIBD
Diagnosis of PIBD can be made on histology if the ratio of presence of
bile ducts to portal tracts is less than 0.4-0.6. But liver biopsy should
contain minimum 5 portal tracts to make the diagnosis of PIBD in a
biopsy specimen.
If the results of biopsy are equivocal (5%) and age is less than 6
weeks, BRIDA scan and or repeat liver biopsy after 10-14 days should
be done. The other modalities used are MRCP and ERCP but all depends
upon the experts available.

Magnetic Resonance Cholangiopancreatography (MRCP)

This is newer noninvasive modality but experts one required for
interpretation of neonatal bile ducts.

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Problem with ERCP is technical failure and non-availability of small
diameter ERCP scopes is most of centers.

Laparoscopy
Laparoscopic visualization of hepatobiliary area has not been popularized
in children but some experts are attempting it. Duodenal intubation:
140 Selected Topics in Pediatrics for Practitioners

Aspiration of duodenal fluid for 24 hours to see for bile is popular

procedure in Japanese centers whereas others have not accepted it. This
can be done during scintigraphy to define the radioactivity in stomach
and duodenal fluid.

Intraoperative Cholangiography(IOC) or
Peroperative Cholangiography (POC)
This is the gold standard to confirm the diagnosis of EHBA, when above
given investigations do not suggest EHBA. In presence of gallbladder
IOC showing dye in duodenum and after clamping the CBD showing
dye in intrahepatic redicles rules out EHBA. On the other hand if dye
is not going to duodenum or there is no extrahepatic biliary tree this
confirms EHBA. There is advantage of taking wedge biopsy of liver.
Kasai’s post-enterostomy can be done simultaneously in EHBA.

Approach to Neonatal Hepatitis

Neonatal hepatitis is most important cause of NCS (60-70%). It is
important to record detail history regarding antenatal, natal and postnatal
events, family history, exposure to various drugs, maturity of the baby,
neonatal sepsis, intrauterine infections, various metabolic and genetic
disorders. Thorough clinical examination is warranted. The clue to the
etiological diagnosis should come from good clinical evaluation of the
case. Infections in our set up are very important cause of neonatal
hepatitis. These include bacterial, viral, protozoal and spirochetal
infections are given in Figure 14.5. If there is direct clue to some metabolic
or a genetic disorders the investigations should be done accordingly. If
the infections have been ruled out reasonably, the next choice is to do
metabolic work up. High index of suspicion to think of these disorders
should be based upon certain clinical pointers like family history of
previous sib death due to similar disorder, repeated hypoglycemia,
seizures, vomiting, failure to thrive, cataract, etc. Preliminary metabolic
work up includes urine for reducing substances like galactose or fructose,
serum alpha-1 anti-trypsin level, thyroid function tests, serum amino
acids, urine amino acid screening, eye examination, urinary succinyl
acetone, serum ferritin, etc. Based upon the suspected diagnosis the
specific enzyme estimation/genetic work up should be done.
In spite of elaborate work in 30-40 percent cases of neonatal hepatitis
the etiology can be defined. This group is labeled as idiopathic neonatal
hepatitis or gaint cell hepatitis. Liver histology shows marked giant cell
reaction. Liver biopsy also gives clue towards metabolic disorders at
times.
 Neonatal Cholestasis Syndrome Practical Approach 141

Treatment
Neonatal Hepatitis
Infections constitute major causative agents for neonatal hepatitis in
developing countries. Bacterial infections must be treated very effectively.
Urinary tract infection remains hidden infection in neonatal period should
be diagnosed and treated energetically. Viral infections persay don’t
require any specific therapy in this age group but protozoal infections
like malaria and toxoplasmosis and congenital syphilis as mentioned in
the Fig. 14.5 should be treated effectively.
Treatment of various metabolic disorders should be started at the
earliest. The offending agent should be withdrawn promptly for example
in case of galactosemia, milk should be stopped immediately to avoid
effect on the developing brain. This is the commonest metabolic disorder
encountered in our center. In case of fructosemia, fructose containing
food items must be withdrawn immediately. Treatment of various
endocrinologic and metabolic disorders should be done accordingly.
Genetic counseling and need of the antenatal diagnosis should be stressed
in the affected families.

Fig. 14.5
142 Selected Topics in Pediatrics for Practitioners

Obstructive Cholestasis
Extrahepatic Biliary Atresia (EHBA)
The necro-inflammation of the biliary tree leads to fibrosis also called
obliterative cholangiopathy exact etiology is not clear is for. EHBA is a
big challenge world-over but it is more alarming problem in developing
countries. This constitutes 30 percent of the NCS seen at our center .The
late presentation of the disease is responsible for development of cirrhosis.
This is a stage when it becomes untreatable and death is inevitable
within 2 years of life. The age of presentation of EHBA cases reporting
at our center given in Table 14.2. Bile flow can be established in 80-90
percent cases after Kasai’s procedure portoenterostomy if done within
60 days of life.12 With the advancing age the bile flow decreases. If the
surgery is done within 2-3 months the bile flow can be established in
40-45 percent cases whereas of surgery done after 3 months of age, the
bile flow can be established in 10-20 percent of cases only. In 85 percent
of EHBA patients, the extrahepatic biliary is fibrosed and needs
protoenterostomy and are called non-correctable EHBA. Fifteen percent
of EHBA may have part of CBD or hepatic duct patient and these
require choledochoduodenostomy and hence called as correctable EHBA.

Table 14.2: EHBA: Age of presentation N 36 PGI

Age in months Number (%)

1-2 6 (16.6)
2-3 8 (22.2)
] 83.4%
>3 22 (16.2)
3-6 13 (36.1)
6-12 9 (25)

This shows that diagnosis of EHBA should be done early and surgery
should be performed within 60 days of life. Best time is 4-6 weeks of life.
Inspite of advancement is surgical skills the outcome is not
encouraging. Even after protoenterostomy 1/3 cases deteriorate in
perioperative period and first year of surgery and may require liver
transplantation, 1/3 develop complications of liver disease during first
decade of life and require liver transplantation whereas 1/3 survive
beyond 10 years of life with abnormal liver functions.
One year survival reported is varying from 30-71 percent. The highest
survival rate is reported by Japanese workers. One year survival in our
country is 25-30 percent. This shows that surgery is not full proof
treatment and needs liver transplantation. Good prognostic factors for
EHBA surgery are surgery done under 60 days of life, minimal or no
fibrosis on histology, good bile flow after surgery and absence of
 Neonatal Cholestasis Syndrome Practical Approach 143

chloangitis in immediate postoperative period or first year of life and

availability of surgical expertise. In our set up late presentation of the
cases (Table 14.1) and chloangitis are the main determinental reasons for
the bleak outcome of these cases.
Choledochal cyst during infancy is also very important cause
cholestasis (6%) and needs surgical treatment.4,5

Liver Transplantation
Liver transplantation has revolutionized the outcome of EHBA worldover.
The indications are failed Kasai’s procedure, progressive liver disease
inspite of successful Kasai’s procedure and late presentation of EHBA
(unoperated). Ten years survival is 85-90 percent in various centers. In
our country this has not picked up because of lack of awareness, poverty,
ignorance, and absence of cadaveric liver transplantation program.

Medical Treatment
Chronic cholestasis is responsible for various life threatening
consequences which need prolonged therapy.

Pruritus
Pruritus is a most distressing symptom. It leads to miserable life in term
of lack of sleep, emotional problems and children become mentally
reackoned. Various treatment modalities in form of use of cholestyramine,
plenobarbitone 5 mg/kg/day, rafampicin (10 mg/kg/day), terfenadine,
UCDA (20-40mg/kg) and phototherapy have been tried with variable
results. UDCA seems to be promising as it is one of choleretic drug.
Some times untreatable and unremitted pruritus becomes sole indication
for liver transplantation.

Malnutrition
Malnutrition is very common and is due to obvious reasons mentioned
in the Figure 14.2. Breastfeeding should be encouraged in these babies.
If anorexia is a prominent feature nasogastric feeding is indicated. The
diet should have 200 calories/kg and protein 1-2 g/kg body weight. The
diet should be constituted by MCT (2-3% calories from PUFA),
carbohydrates (glucose polymers), minerals, trace elements and vitamins.
MCT rich available diets are coconut oil, simy1 MCT, Pregestimil and
Portagen. All vitamins should be given in double the daily
requirement.10,11
144 Selected Topics in Pediatrics for Practitioners

Vitamin A
Vitamin A should be given 2500-5000 IU/day. Monitor the vitamin level.
If blood level is less than 30ug/dl increase the oral dose by 10 folds or
gives 50,000 IU IM.

Vitamin D
Daily 400-1200 IU of vitamin D is recommended. This can be given in
form of 40,000 IU IM monthly. 25-hydoxycholecalciferol 5-7 µg/kg can
be given daily. Monitor serum calcium, phosphate and alkaline
phosphatase and X-ray wrist at 2 months internal.

Vitamin E
Vitamin E deficiency is now recognized very oftenly since the age of the
children with cholestasis is increasing. The dose of vitamin E
recomendced is 15-200mg daily. Serum monitoring is mandatory. If levels
are lower side than higher dose should be given. Six monthly neurological
and yearly eye examination are required.

Vitamin K
In case of prolonged cholestasis with steatorrhea vitamin K 5 mg IM
monthlty should be given. Treatment of other complication of liver disease
like ascites, portal hypertension, vericeal bleed and encephalopathy
should be done accordingly.10

Prognosis and Outcome

Prognosis of NH is very good if diagnosed early and appropriate
treatment is instituted depending upon the etiology. In idiopathic neonate
hepatitis 70-80 percent recover daily 10-20 percent may have progressive
liver disease and very small percentage of 1-2 percent may develop
cirrhosis. Death occurs due to sepsis, bleeding or acute liver failure. In
EHBA even after successful portoenterostomy 1/3 die during 1 of year
operation, 1/3 die by 10 years of age whereas 1/3 survive after 10 with
some compromised liver functions. With liver transplantation survival
of EHBA has improved to 90 percent in best centers.

Liver Transplantation
Liver failure due to metabolic conditions in neonatal period and infancy
is difficult to manage medically. Liver transplantation have changed the
outcome in western world.
To summarise the scenario of NCS in India is disappointing at present
because of late referral of the cases to centers where facilities to diagnose
metabolic diseases and EHBA are available. This has been shown in
Table 14.2. More than 80 percent of EHBA cases come for treatment
 Neonatal Cholestasis Syndrome Practical Approach 145

when they have already crossed 2 months of age as show in Table 14.2
when it is difficult to establish the bile flow. The mistake is at various
levels starting from undergraduate training to postgraduate training in
pediatric medicine, unawareness about the seriousness of the problem,
wastage of time on making diagnosis and treatment. These are not
correctly practised in peripheral hospital/medical college hence delay
in referral of these cases.
The algorithm given in Figure 14.6 shows reasons for late referral of
EHBA in India. There is a lack of surgical expertise also to handle
EHBA. We have the facilities of liver transplantation in our country but
cost factor and non-availability of cadaveric liver are main hinderances.
In this context parents can help by giving piece of their liver to their
own produced baby. Hence, there is need of “Yellow Alert” nation wide
to detect these cholestatic babies and early referral to well-equipped
tertiary care center where facilities for diagnosis and treatment of these
babies are available so there is need for an Indian effort to detect
cholestatic babies, to make early diagnosis and prompt treatment to
avoid occurrence of end stage liver disease given in Figure 14.7.

Fig. 14.6: Algorithm-III late referral of EBHA in India

146 Selected Topics in Pediatrics for Practitioners

Fig. 14.7: Need for an Indian effort cholestasis ASIS of infancy

REFERENCES
1. Whitington PI. Chronic cholestasis of infancy. Ped Clin Nor Am 1996;43:1-26.
2. Shah HA, Spivak W. Neonatal cholestasis: New approaches to diagnostic
evaluation andtherapy. Ped Clin Nor Am 1994;41:943-66.
3. McEvoy CF, Suehy FJ. Biliary tract disease in children. Ped Clin Nor Am
1996;43:75-98.
4. Chhabra M, Poddar U, Thapa BR, Singh K. Spectrum of cholestasis of infancy.
Indian J Gastroenterol 1996;15:(Suppl. 1) A 73.
5. Poddar U, Thapa BR, Chhabra M, Rao KLN, Mitra SK, Singh K. Choledochal
cysts in infants and children. Indian Pediatr 1998;35:613-18.
6. Paltiel HJ. Imaging of Neonatal cholestasis. Semin Ultrasound CT and MRI
1994;15:290-305.
7. Kotb MA, Sheba M, EL Koofy N et al. Evaluation of “Triangular cord sign”
in the diagnosis of biliary atresia. Pediatrics 2001, 108:416-20.
8. Lai MW, Chang MH, Hsu SC, Hsu HC, Cheng TS, Kao CL, Lee CY. Differential
diagnosis of extrahepatic biliary atresia from neonatal hepatitis: a prospective
study. J Pediatr Gastroenterol Nutr 1994;18:121-17.
9. Chardot C, Carton M, Spire-Bendelae N et al. Is Kasai’s operation still indicated
in children older than 3 months diagnosed with biliary atresia?
J Pediatr 2001, 138:224-28.
10. Thapa BR. In Sachdev HPS, Choudhary P (Eds): Role of nutrition in liver and
biliary disorders in nutrition in children. Developing country concerns (1st
edn). Cambridge Press, Kashmeregate: Delhi 1994;376-89.
11. Kader HH, Balisteri WF. In Re Behrman, RM Kliegman, HB Jenson (Eds):
Cholestasis from Nelson Textbook of Pediatrics. Saunders Company (17th
edn). 2003;1314-19.
 15
Constipation and Encopresis
in Infants and Children
BR Thapa

Constipation is a symptom of underlying disorder and is more common

in males as compared to female and children. It is a very common
problem in pediatric age group. 10-25 percent of all patients attending
pediatric gastroenterology clinics are constituted by various fecal
elimination disorders. About 1.3-5 percent of children suffering from
chronic constipation have problem of encopresis. Chronic constipation
is a real challenge to the parents, children as well as for the pediatricians
to understand and to treat it effectively. The presence of encopresis adds
to the parental anxiety and has a great impact on the overall development
of the child in the society. This warrants a meticulous and well planned
approach to manage a child with constipation.1

DEFINITIONS
Constipation
Constipation is defined subjectively a feeling of unsatisfactory evacuation.
The other accompaniments could be passage of too small stool, too hard
stool, too difficult to expel, too frequent and incomplete evacuation, but
the accepted definition of constipation is passage of stools twice or less
per week.

ENCOPRESIS/SOILING/INCONTINENCE
Encopresis
Encopresis is the in-voluntary passage of formed, semiformed or liquid
stool in the child’s underwear. Largely this is considered to be functional
when there is no organic or anatomic cause or medication responsible
for it after the age of 3-4 years. This is equivalent to enuresis in children
and is also called overflow incontinence when there is chronic
constipation. Before this age it is very difficult to recognize because,
diapers are used and moreover, voluntary control on the act of defecation
148 Selected Topics in Pediatrics for Practitioners

may not be achieved. This emphasises the fact that encopresis could be
functional or overflow incontinence.

Fecal Soiling
Fecal soiling is any amount of stool deposited in the underwear,
independent of whether an organic or anatomic lesion is present.

Fecal Incontinence
Fecal incontinence is fecal soiling in the presence of an organic or anatomic
lesion such as anal malformation, anal surgery, anal trauma,
meningomyelocele and other neurological and muscle diseases affecting
the anorectal area and perineum. There is no retaining capacity due to
lack of reflexes involved in retention of stool and act of defecation. But
some authors have used these terms interchangingly in the literature.1

CLASSIFICATION
This is not clear from the literature. For better understanding of the
problem the suggested classification is given in Table 15.1. There is no
ambiguity to understand the congenital and acquired constipation. Acute
constipation is defined when it is of shorter duration possibly less than
4 weeks. On the other hand, when the duration of constipation is more
than 4 weeks and is present for months and years is labeled chronic
constipation. This may or may not be associated with megarectum,
megacolon and encopresis.
Table 15.1: Classification of constipation
1. Depending upon the age of onset
a. Congenital constipation
b. Acquired constipation
2. Depending upon the duration
a. Acute constipation (simple)
b. Chronic constipation
• No megarectum, megacolon and encopresis
• Associated with megarectum and megacolon
• Associated with encopresis

PATHOPHYSIOLOGY OF CONSTIPATION
Normal Bowel Habits
The normal frequency of stools varies from 3 times per day to 3 times
per week. But this may be as high as 4-10 times during breastfeeding
period in infancy. Toddlers may pass stools 3-5 times per day but as the
age advances the transit time increases and normal adulthood frequency
of 1-2 times per day is achieved after 5 years of age.
 Constipation and Encopresis in Infants and Children 149

Bowel Training
Normal bowel training should be started at the age of one year when
infant starts walking. Regular timing and passage of at least one stool
per day are essential for the normal function of the bowel. For this use
of appropriate potty or toilet where a child can sit in squatting position
is required. Mother should ensure that child sits comfortably on the
lavatory seat without fear.
Mother should use one word for defecation and if baby repeats this
is a good sign. Child should be made to sit for 5-10 minutes. Normally,
children start attending toilet independently by the age of 2-3 years.
Problems in the bowel training can arise because of dietary changes, low
fiber diet, formula feeds, anal fissure, intercurrent illnesses, travel, moving
to new home, family dysfunction, birth of sibling, erroneous parents
expectation, family problems, failed toilet training, unresolved stress in
school, changing of school, privacy, drugs and various neurological
disorders. Most of the times these precipitating factors are responsible
for onset of constipation with some functional overlay.

Pathogenesis of Constipation
Constipation during childhood is confluence of variations in physiological
tendencies like developmental transitions, environmental factors and
parental response. Most of the times constipation is a problem in toddlers
and this may become passive if tackled in time. There is always a
precipitating cause.

Infancy
During infancy the constipation is mostly pathological due to
Hirschsprung’s disease, anorectal problems, mental retardation or another
anatomical abnormalities. This may also be due to formula feeding and
lack of cereal supplementation after 4 months of life.

Toddlers/Preschool Children
In toddlers the most important factor is the painful act of defecation due
to anal fissure. The anal injury occurs due to passage of hard stool and
later on this gives rise to retention and pain cycle given in Figure 15.1.
This goes on and results into chronic constipation. Children start adopting
different postures to evacuate. This leads further injury to anal canal. As
they start going to school other confounding factors come in operation.
This results into stool impaction and leads to megacolon and megarectum
to accommodate large volume of stool. The retention of large volume of
stool is responsible for pain abdomen and encopresis or soiling in the
underwear subsequently.
150 Selected Topics in Pediatrics for Practitioners

Fig. 15.1: Pain a common factor in constipation in toddlers

School Children
The lack of privacy and positive reinforcement leads to problem of
chronic constipation. Psychologically children are withdrawn and develop
other functional problems also.2,3 This is more common in female children
who don’t find appropriate hygienic bathrooms in the school. Various
other causes of constipation in children are given in table 2 and 3.

Table 15.2: Etiology of acute constipation in infants and children

Infants
• Change of diet
• Formula feeds
• Milk based diet
• Anal fissure
• Inflammation in perianal area
• Boil
• Dermatitis
• Drugs: Opiates, Janam gutti, etc.
Toddlers and older children
• Change of diet
• Change of place
• Traveling
• Anal fissure
• Boil
• Abscess
• Infected hemorrhoids
• Dermatitis
• Low fiber diet
• Drugs
 Constipation and Encopresis in Infants and Children 151

Table 15.3: Etiology of chronic constipation with or without mega- rectum,

megacolon or encopresis
a. Congenital
• Anorectal defects
— Anal stenosis
— Anal atresia
— Imperforate anus
— Anteriorly displaced anus
• Neurogenic
— Myelomeningocele
— Spina bifida
• Colonic neuropathies
— Hirschsprung’s disease
— Intestinal neuronal dysplasia
b. Acquired constipation
• Idiopathic or functional 90-95%
• Anal lesions
— Anal fissures
— Abscess
— Strictures due to IBD, TB
— Anal surgery or trauma
• Neurological conditions
— Cerebral palsy
— Hypotonia
— Mental retardation
— Tumor of spinal cord
• Metabolic
— Hypokalemia
— Hypomagnesemia
— Hypophosphatemia
— Hypercalcemia
— Cystic fibrosis
— Celiac disease
• Endocrine
— Hypothyroidism
— Multiple endocrine neoplasia IIB (MEN)
— Diabetic mellitus
— Hyperparathyroidism
• Drug induced
— Antimotility drugs
— Anticholinergics
— Antidepressants
— Antihypertensives
— Anticonvulsants
— Opiates
— Codeine
— Antacids
— Phenothiazines
— Methylphenidate
• Low fiber diet

Association of Chronic Constipation

Children suffering from recurrent abdominal pain (RAP) 50 percent may
be constipated and 20 percent of them may show psychiatric problems.
152 Selected Topics in Pediatrics for Practitioners

With the impaction of stools other associations are enuresis, UTI, palpable
mass, soiling/encopresis/overflow incontinence, finger evacuation,
solitary rectal ulcer, rectal prolapse, irritability, scissoring of legs, passage
of stool while standing (unphysiological way to pass stools). Usually
there is loss of appetite and poor weight gain.3,4

Approach to Constipation
While taking history, special attention should be paid towards the stool
habits, which include character of stools in the toilet, in the underwear
and stool withholding maneuvers. Age of onset of constipation is also
important. Constipation starting from neonatal life gives clue towards
developmental anomalies of anorectal area or colon. Delayed passage of
meconium gives clue of Hirschsprung’s disease. Associated abdominal
pain may be the sole symptom of constipation in 50 percent children
with RAP. It is important to enquire about dietary habits of the child.
Consumption of excess of milk, juices and/or other drinks, junk foods
and bakery products may lead to constipation. In the modern era children
largely depend upon low fiber diet and this becomes important factor
for onset of constipation. Less consumption of cereals, pulses, vegetables
and fruits can result into constipation. Inadequate diet and low fiber
diet result into less production of stool. One must also enquire about the
associated conditions like enuresis, UTI or any psychiatric problems.
There is loss of appetite due to delayed stomach emptying and slow
transit time due to cologastric reflex. There may be poor weight
gain.4-6
Patients should be thoroughly examined especially abdomen and
anal region. Rectal digital examination should be carried out. In presence
of anal fissure digital rectal examination should be avoided because this
can enhance the anal injury. Neurological examination including perianal
sensation testing should be done. Investigations in case of simple
constipation are not required. Plain X-ray abdomen can give idea about
the fecaliths in whole of colon and rectum. Investigations like anorectal
manometry, surface perianal electromyography, intestinal transit
determination, defecography and defecation stimulation are not
commonly required. These are needed in intractable situations when
rectoanal dyssynergia is suspected. Full thickness rectal biopsy to
demonstrate the absence of ganglion cells is required for the diagnosis
of Hirschsprung’s disease. Barium enema study may help to pickup
Hirschsprungs’s disease. The systematic diagnostic approach4,5 is given
in Figure 15.2.
 Constipation and Encopresis in Infants and Children 153

Fig. 15.2: Algorithm for the application of diagnostic tests in

constipated children. ACHE acetylcholine stain
Treatment
Treatment of constipation is aimed at
1. Treating the cause,
2. Evacuation
3. Maintenance therapy.
The treatment of underlying precipitation factor and evacuation
should start simultaneously. After evacuation, the passage of normal
stools should be maintained.3

Simple Acute Constipation

Simple mild constipation is very common in children. Parents must be
educated and reassured that it is not pathological. One has to eliminate
154 Selected Topics in Pediatrics for Practitioners

the precipitating cause. Treat local causes like anal fissure, boil or
dermatitis effectively. Procedures like enemas, finger evacuation/
disimpaction, finger dilatation and frequent use of suppositories should
be avoided. But encourage use of high fiber diet in terms of cereals,
pulses, vegetables and fruits. Initially laxatives can be used. Encourage
toilet training simultaneously. Laxatives can be given for 7-10 days but
prolonged use should be discouraged.

Treatment of Chronic Constipation and Encopresis

Treatment of chronic constipation is possible by multimodality approach1
as given below.

Initial Counseling
This is the education of parents and child regarding normal feeding,
normal anatomy, bowel functions and transitions, process of stooling,
definitions of medical terms, model for development of bowel dysfunc-
tion and the purpose of each intervention. Parents should also be
explained about the problem to be encountered, need for persistence to
read the literature, develop caring relationships, resolve issues of blame,
guilt or punishment, stress the need for behavioral modification tech-
niques and need for long follow-up.

Bowel Cleansing/Disimpaction
This is very important to have clean bowel free of retained/impacted
stools. This will take care of overflow incontinence/soiling.

Enemas
Hypertonic phosphate enemas once or twice a day can clear the rectum
effectively. The dose recommended is 6 ml/kg/day. Saline enema is less
effective but can be used. This takes longer time to clean the colon. Plain
tap water and soap water enemas are not to be used in children.

Lavage
Total bowel wash is very effective to clear whole of colon. This can be
done with normal saline or polyethylene glycol electrolyte solution in
the dose of 14-40 ml/kg/hour for 2 hours wait till the returns one clear.
Metaclopramide (5-10 mg) should be given ½ hour before the lavage to
avoid vomiting. Sodium phosphate solution can be used. In case child
is not able to take enough fluids orally, can be given through nasogastric
tube.
 Constipation and Encopresis in Infants and Children 155

Suppository
Glycerine or bisacodyl suppositories can be tried in younger children
and may evacuate rectum effectively. But this is required repeatedly.

Purgation
Large dose of mineral oil (liquid paraffin) or castor oil or osmotic agents
can effectively evacuate rectum. Usually repeated doses are required.

Surgery
Surgical disimpaction is required rarely in severe constipation, failed
medical treatment, mental retardation and fearful situation with poor
compliance. Surgery is the definite treatment of Hirschsprung’s disease
(HD) and other anorectal congenital anomalies in children.

Maintenance Therapy
The goals of maintenance therapy are:
1. To maintain adequate frequency
2. To avoid continued passage of large stools, and
3. To prevent with holding/retention of stools. Retraining medications
include stool softeners with one bulk-forming agent like isabugol or
bran. Other laxatives used are milk of magnesia, agarol, lactulose,
etc. in the dosage of 1-3 ml/kg body weight. These should always
be given twice a day. The maintenance therapy has to continue for
4-6 months depending upon the response. Routine use of bisacodyl,
castor oil and phenolphthalein is not recommended in children. These
stimulate the peristalsis, active electrolyte transport and fluid
movements.
Cisapride a prokinetic agent can be used in paraplegics, pseudo-
obstruction, diabetics, chronic constipation, etc. Prebiotics and probiotics
have been shown to be effective but more studies are required.
Combinations of various agents is effective to avoid recurrence of
constipation. The most commonly used drugs/agents along with dosage
and side effects are given in Table 15.4.

Dietary Modification
Encourage breastfeeding during early infancy and cereal supplementation
should be done after 4 months of life. Diets rich in high fiber are bran
based cereals, pulses, fruits, vegetables, etc. For older children and adults
daily intake of 20 g of bran is quite effective to avoid constipation.
Intake of plenty of fluids is encouraged. Excess of drinks inform of milk,
sugar, water, juices and cold drinks to be avoided. Bakery products and
156 Selected Topics in Pediatrics for Practitioners

Table 15.4: Commonly used oral medications in childhood constipation

Agents Dosages Side effects

Osmotic
Lactulose/sorbitol 1-3 ml/kg/dBD Bloating, cramps, diarrhea
Magnesium citrate 1-3 ml/kg/d (< 6 y); 100-150
ml/d (6-12 y); 150-300 ml/d Hypermagnesemia,
(> 12 y) hypophosphatemia, and
secondary hypocalcemia
Magnesium hydroxide 1-3 mL/kg of 400 mg/5 mL
(available as liquid)
Lubricant
Mineral oil (liquid paraffin) 1-3 ml/kg/d (maintenance); Aspiration risk lipoid,
15-30 ml/yr of age pneumonia
(disimpaction)
Lavage
Polyethylene glycol 5-10 ml/kg/d (maintenance); Nausea, vomiting, cramps,
25 mL/kg/h via nasogastric tube risk of aspiration
till clear (disimpaction)
Stimulants
Senna 2.5-7.5 ml/d (2-6 y); 5-15 Melanosis coli, hepatitis
ml/d (6-12 y)

junk foods to be discouraged. Mechanism by which dietary unabsorbed

carbohydrates known as prebiotics increase the stool bulk is given in
Figure 15.3.

Retraining
There should be positive reinforcement for toilet sitting and defecation.
Toilet timing should be regular. Child should sit in squatting position
for 5-10 minutes once or twice a day after the meals to take advantage
of gastrocolic reflex. Positive reinforcement at home and by the physician
is very important. Parents should be prepared to have verbal acclaim
and selective awards for desired behavior, initiation of toileting, use of
toilet, production of stool, acknowledging the cleaning after defecation
and for repeated successes.5

Biofeedback
Biofeedback is required when other measures are not working and there
is anorectal dyssynergia. This helps in relaxation of EAS and levator ani
muscles. This is only possible above 5 years of age because co-operation
of patient is very important. It is effective in 50-80 percent patients. Take
the benefit of conditioning reflex in morning and evening like to move
infront of toilet, to drink water, put the tap on and sitz bath.
Multidisplinary behavioral treatment is effective in chronic constipation
and defecation process in HD in children.6
 Constipation and Encopresis in Infants and Children 157

Fig. 15.3: Mechanism by which dietary unabsorbed carbohydrates

(prebiotics) may increase the stool bulk

Follow-up
Long follow-up is required. In case the progress is very good, the
treatment can be weaned off after 4-6 months, but rest of the protocol
is term of high fiber diet and toilet training should continue for 2-3 years
to avoid relapse. Appropriate psychiatric consultation should be taken.
If there is atypical presentation or poor response, pathological cause
must be ruled out.

Outcome and Prognosis

Outcome with appropriate above mentioned therapeutic modalities is
excellent in 45-100 percent of individuals. Moderate response may be
seen in 20-30 percent whereas 25-35 percent may have failure. Good
prognostic indicators are better compliance, adequate intake of high
roughage diet and self-confidence to achieve the success. Poor prognostic
indicators are hearing disabilities, disobedience, fearlessness, school time
soiling, teenage occurrence, mental retardation, severe motor disability,
associated disorders and neurogenic cause. In a recent study this has
been shown that 30 percent of children suffering from constipation
continue to be constipated during puberty.7
158 Selected Topics in Pediatrics for Practitioners

Prevention
Prevention of colonic dysfunctions have received much less attention
but attending pediatrician can play important role by providing
anticipatory counseling in terms of appropriate feeding advice, high
fiber diet, interpretation of normal bowel habits, counseling life issues
of the child and early detection of problem and intervention.
In summary the approach to the treatment of constipation is
summarized in Figure 15.4.

Fig. 15.4: Management of constipation summarised

REFERENCES
1. Seth R, Heyman MH. Management of constipation and encopresis in infants
and children. Gastroenterol Clin Nor Am 1994;23:621-36.
2. Loening Baucke V. Encopresis and soiling. Pediatr Clin Nor Am 1996;43:279-
98.
 Constipation and Encopresis in Infants and Children 159

3. Lennard Jones JE. Constipation form Sleisenger and Fordtran’s Gastrointestinal

and liver disease. Feldman M, Scharschmidt BF and Sleisenger MH (Eds). WB
Saunders Company: Philadelphia 7th edition volume I, 2002;181-10.
4. Loening-Baucke V. Chronic constipation in children. Gastroenterology
1993;105:1557-64.
5. Yousef NN, Di Lorenzo C. Childhood constipation evaluation and treatment.
J Clin Gastroenterol 2001;33:199-205.
6. van Kuyk EM, Brugman-Boezeman ATM, Wissin K et al. Defecation problems
in children with Hirschprung’s disease: a prospective controlled study of a
multidisciplinary behavioral therapy. Acta Pediatr 2001;90:1153-59.
7. van Giukel, Reitsma JB, Buller HA et al. Childhood constipation longitudinal
follow-up beyond puberty. Gastroenterology 2003;125:357-63.
 16
Urinary Tract
Infection in Children
M Vijayakumar

IMPORTANCE OF UTI
By definition it is infection of the urinary tract as identified by a positive
urine culture. UTI today, assumes significant position among FUO’s
(Fever of Unknown Origin) and hence a fair suspicion and careful history
are mandatory. E coli, Klebsiella, Pseudomaonas, Proteus and Enterococci are
responsible for 90 percent of acute UTI and 70 percent of chemical
infection. Early diagnosis, prompt treatment, investigation for urinary
tract malformations are necessary; otherwise it may result in renal
parenchymal damage causing hypertension and chronic renal failure at
a later stage. One percent of boys and 3-5 percent girls below the age
of 14 years have the risk of developing UTI. In infancy the male to
female ratio is 3-5:1 beyond 1-2 years there is female preponderance
with male to female ratio of 1:10. UTI and the presence of vesicoureteric
reflux (VUR) with intrarenal reflux (IRR) are the common risk factors
involved in the causation of renal scars. Associated anomalies like
posterior urethral valve, neurogenic bladder, etc. further modifies the
outcome of UTI. A growing kidney afflicted with UTI can result in
diminished size of the kidneys. Recurrent UTI can predispose to renal
stones, hypertension and renal failure as mentioned. This is a treatable
condition leading to severe morbidity. UTI and parenchymal damage is
the result of interaction between the predisposing factors in the child
and virulence of the pathogens. Ninety percent of acute infection and
70 percent of chronic infections are due to E.coli and Klebsiella,
Pseudomonas, Proteus and Enterococci are the other common pathogens.

DEFINITIONS
Certain terminologies in UTI are important:
1. Acute UTI (Significant Bacteria): Colony count > 105/ml of a single
organism in a midstream clean catch sample.
2. Recurrent UTI: Second attack of UTI.
 Urinary Tract Infection in Children 161

3. Simple UTI: First attack of UTI showing no renal tract abnormality

or recurrences with appropriate and adequate treatment.
4. Complicated UTI: First attack of UTI not resolving with conventional
therapy, recurrent UTI and UTI associated with renal tract anomalies.
5. Asymptomatic bacteriuria: Presence of significant beacteriuria on two
or more stream clean catch sample.
6. Lower tract UTI: Involvement of urethra and bladder presenting as
low-grade fever, dysuria, urgency, frequency. It is also known as
dysuria frequency syndrome.
7. Upper tract UTI: Child presenting with high-grade fever > 38.5oC,
systemic toxoicity, persistent vomiting and renal angle tenderness
with positive acute phase reactants.

CLINICAL FEATURES
Neonates and Young Infants
The most common presentation is with features of septicemia. Failure
to thrive, vomiting and diarrhea are non-specific symptoms. Unexplained
fever with foul smelling urine should arouse suspicion of UTI.

Older Children
Cystitis: Dysuria, frequency and hypogastric pain upper tract UTI: Fever,
toxicity, constitutional symptoms and renal angle tenderness. Distal
urinary tract anomolies: Dribbling, prolonged voiding, straining, crying
during micturition and poor urinary stream.
Voiding dysfunction: Diurnal incontinence, urgency, frequency and
squatting.
Diagnosis: Gold standard is positive culture in properly collected urine.
Generally a colony count of 105/mm3, i.e. > 1,00,000 is considered
diagnostic but > 10,000 and < 1,00,000 may also be considered significant
following appropriate antibiotic therapy or in polyuric state.
Careful history pertaining to the above symptomatology is mandatory
along with detailed clinical examination, viz. BP recording, abdominal
examination-look for renal/bladder mass and loaded colon, examination
of genitalia for phimosis, tight fore skin and vaginal synechiae, nervous
system evaluation when nocturnal enuresis, dribbling and incontinence
are presenting symptoms.

Diagnosis
Gold standard investigation needed to document UTI is a positive culture
of properly collected urine.
162 Selected Topics in Pediatrics for Practitioners

Collection of Urine
Midstream urine specimen is the practical way of collecting urine in
older children. In children upto 2-3 years of age suprapubic aspirate is
ideal. Catheter sampling is reserved only when catheterisation is done
for non-culture purposes like catheterisation for doing VCU, etc. Bag
specimens are useful only for documenting a negative culture.
Urinalysis: Urinalysis may show mild proteinuria, leukocyturia (>5
leukocytes/HPF in centrifuged sample or > 10 leukocytes/mm3 in an
uncentrifuged sample), bacteria on Gram-stain and positive leukocyte
esterase and nitrate test by dipstick.
Urine culture significance: A colony count of > 100/mm3 is significant
bacteriuria, when midstream urine is used for culture. Urinary pathogen
in any number can predict UTI, if suprapubic aspirate of urine is the
sample. A colony count of less than 10,000 is usually taken as insignificant.
A colony count of > 10,000 and < 1,00,000 can still be considered
significant, if urine is taken after child has been subjected to appropriate
antibiotic therapy in initial days of fever or in polyuric state.

History and Clinical Examination

Once UTI is documented in a febrile child every attempt should be
taken to note the following:
• History regarding bowel and bladder habits: Constipation, encopresis,
nocturnal enuresis, straining, narrow stream of urine, dribbling,
incontinence, hematuria, passage of stones and mud, etc.
• Degree of toxicity, dehydration and ability to retain oral intake.
• Blood pressure measurement.
• Abdomen examination for renal and bladder mass as well as loaded
colon.
• Examination of genitals for phimosis, tight foreskin and vaginal
synechiae.
• Nervous system evaluation in children with nocturnal enuresis,
dribbling and incontinence.

Initial Evaluation
Estimation of blood urea, serum creatinine, complete blood count, ESR,
CRP and blood culture. Also, USG evaluation in initial stage. When
further needed DMSA scan followed by VCUG.
• Blood urea, serum creatinine, complete blood count, ESR, CRP
estimation and blood culture in every child with febrile UTI.
• USG evaluation in the initial stage itself in febrile UTI.
 Urinary Tract Infection in Children 163

Common Guidelines in Management

• Urine culture with antibiogram is the ideal way to disgnose and treat
UTI.
• All UTIs are treated only as upper tract infection in children.
• Single dose or short-term (3-5 days) chemotherapy is not advocated
in children.
• In vitro and in vivo sensitivity are not the same in some instances
• No Polypharamacy except in complicated UTI and septicemia where
it is need.
• Dose modification is needed for drugs excreted mainly through kidney
in the presence of renal failure.
• Chloromycetin as a drug for UTI is avoided as only waste metabolic
end products reach the kidney.
• Nalidixic acid and nitrofurantoin are reserved only for chemo-
prophylaxis as they are not useful in acute UTI.
• Amoxicillin is better than ampicillin due to its better concentration
in urine.
• Dosage of gentamicin is 1 mg/kg/dose to treat simple UTI due to
its high concentration in urine.
• 10-14 days treatment with repeated culture on 7th day if child is
recovering or on 3rd day if child is not recovering is mandatory.
• Children with complicated UTI and suspected upper UTI are treated
with parenteral antibiotics. Oral therapy is useful in simple UTI and
in children above three months of age with no toxocity.
• On diagnosing UTI ampicillin or amoxicillin, cephalexin and
cotrimoxazole is started in uncomplicated UTI. Drugs are modified
with antibiogram. Gentamicin, cefotaxime, ceftrioxone and Amikacin
is used in the initial phase itself in complicated UTI and modified as
per antibiogram.
• Quinolones are not used routinely in childhood UTI and are reserved
for complicated and recurrent UTI. They are used with caution in
chidren.
• Single night dose of cotrimoxazole (1-2 mg/kg of trimethoprim),
cephalexin (10 mg/kg) and nitrofurantoin (1-2 mg/kg) are the
common drugs used for chemoprophylaxis.
• Chemoprophylaxis play a major role in the management of recurrent
and conplicated UTI.
Subsequent Evaluation
Urine Culture
Urine culture at frequent intervals is needed in recurrent and complicated
UTI. IF fever occurs without focus, urine culture is mandatory as fever
may be due to UTI.
164 Selected Topics in Pediatrics for Practitioners

X-ray KUB
Cab be done during acute UTI itself if needed. Bony abnormalities of
spine like spina bifida, radio-opaque stones and features of bony
deformities at the pelvis can be identified.

USG Abdomen
Usually done during initial phase of febrile UTI. If not done at that time,
every child with documented UTI should have USG abdomen done at
least on subsequent evaluation.

Voiding Cystourethrogram
Voiding cystourethrogram (VCUG) is done in every child with febrile
UTI in less than 5 years old and also in recurrent UTI, even if UTI is of
afebrile nature provided the culture is taken with adequate precautions.
VCUG in a child above 5 years can be done with a positive USG or a
positive DMSA scan. VCUG is not done during acute phase for the fear
of inducing septicemea. After controlling infection and making the urine
sterile, child is started on chemoprophylaxis. Usually after 15 days of
chemoprophylaxis, VCUG is done with 1 mg/kg/dose of parenteral
gentamicin chemoprophylaxis given one hour before catheterization for
VCUG.

DMSA Scan
This has become the gold standard investigation in documenting acute
pyelonephritis. This can be done during acute phase of UTI and even
in the presence of renal failure. Repeat scans are needed at 6,12,24 months
and later as preneed to assess the resolution of scars as well as occurrence
of new scars. This test is also useful in culture negative pyelonephritis,
which is being documented frequently. When VCUG shows VUR, where
DMSA is suggestive of acute pyelonephritis or with multiple scars direct
radionuclide cystogram should be done. The disadvantage of
radionuclide cystogram is that posterior urethral anatomy is not
delineated as the name implies and hence will miss posterior urethral
abnormalities, which is more common in males. This test can be done
in females as a screening procedure as posterior urethral anomalies are
not common.

DTPA Scan
This radionuclide scan is commonly used to assess the obstruction at
PUJ level and function of individual kidneys even in the presence of
renal failure where intravenous urogram (IVU) cannot be done.
 Urinary Tract Infection in Children 165

Intravenous Urogram
Availability of DMSA and DTPA scans has removed the need for IVU
in the evaluation of UTI in most of the instances. In conditions like
megaureter and to correctly assess the level of obstruction as in ureteric
stones, IVU is still found useful.

GUIDELINES FOR DIAGNOSTIC RADIOLOGY

Every child, male or female less than 5 yers with documented febrile
UTI should have USG abdomen, DMSA scan followed by VCUG.
Children above 5 years of age with febrile UTI will have USG abdomen
and DMSA. VCUG is done if scar is present in DMSA or pelvicalyceal
abnormality is present in USG or if DMSA facilities are not available.
Children of any age with recurrent afebrile UTI need USG evaluation.
Further evaluation is decided as per USG findings or associated urinary
symptoms like dribbling. Ofcourse one should be definite about culture
being done with proper precautions.

CHEMOPROPHYLAXIS
Antibiotic prophylaxis is usually recommended under the following
situations:
1. Following treatment of acute UTI in children less than 5 years of age,
awaiting imaging studies.
2. Chidlren with VUR
3. Patients with renal scars following UTI even if reflux is not
demonstrated. If repeat DMSA is better after 1 year or if radionuclide
cystogram or MCU repeated 6 months later is normal,
chemoprophylaxis can be discontinued.
4. Children with frequent febrile UTI (3 or more episodes in a year)
even if urinary tract is normal on evaluation.
Duration of therapy is individualized. Majority will need it for two
years. Ususally chemoprophylaxis is not indicated in children with
urinary tract obstruction like posterior urethral valve or urolithiasis
wherein the chance of colonization of resistant organisms is more.

ASYMPTOMATIC BACTERIURIA
Frequency of asymptomatic bacteriuria occurring in children is about
1 percent in girls and 0.05 percent in boys. History should be taken for
failure to thrive, abdominal pain, unexplained febrile episodes, voiding
dysfunction or constipation to detect abnormalities warranting appro-
priate management. Low virulence E.coli is the most common organism
detected. Renal injury usually does not occur. Attempts at eradication
166 Selected Topics in Pediatrics for Practitioners

can lead to symptomatic infection with more virulent strains. An USG

abdomen alone to rule out common anomalies can be done to be definite
in our approach.

CONCLUSION
UTI in a child is different from adult as it has future consequences if not
identified early, treated adequately, evaluated properly and followed up
actively.

COMMON GUIDELINES IN THE MANAGEMENT

1. Ampicillin or amoxicillin, cephelaxin and co-trimaxazole are drugs
of choice in uncomplicated UTI. Gentamicin, Cefotaxime, Ceftrioxone
and Amikacin in initial phase itself in complicated UTI. Both regimens
may be modified according to antibiogram susceptibility.
2. 10-14 days is the duration of therapy. Repeat culture on 7th day if
child is recovering and on 3rd day if not recovering.
3. Quinolnes are reserved only for complicated/recurrent UTI with
caution.
4. Amoxycillin is preferred to ampicillin because of its better urinary
concentration. Dose of gentamicin is 1 mg/kg/dose, chloromycetin
is avoided; nitrofurantoin (1-2 mg/kg), co-trimoxazole (1-2 mg/kg
of trimethoprim), cephalexin 10 mg/kg in a single night dose are
useful in chemoprophylaxis in recurrent and complicated UTI.
UTI in children merits early diagnosis, prompt and appropriate
treatment with proper evaluation and follow-up.

BIBILIOGRAPHY
1. M Vijayakumar. Urinary Tract Infections in Children in Proceedings of Pediatric
Update 2003, IAP Kancheepuram CME; 2003;54-55
 17
Acute Nephritis and
Nephrotic Syndrome
P Ramachandran

ACUTE NEPHRITIS
Acute nephritic syndrome (ANS) refers to a clinical presentation of
hematuria, oedema, oliguria and hypertension of varying severity. Acute
post-streptococcal glomerulonephritis (APGN), which occurs following
streptococcal infection, is the classical example of ANS and the
commonest cause of ANS in our country.

ETIOLOGY
APGN follows infection of throat or skin with ‘nephritogenic’ strains of
group A beta hemolytic streptococci. Usually APGN occurs about 7 days
to 21 days after the onset of streptococcal infection.

CAUSES OF ACUTE GLOMERULONEPHRITIS

1. APGN (acute poststreptococcal glomerulonephritis)
2. Following other infections: Staphylococcus, S. pneumoniae, gram-
negative bacteria, Hepatitis B, other viral diseases, infective endo-
carditis.
3. Other glomerulonephritides of unknown etiology:
• Membranoprofilerative GN
• Rapidly progressive GN
4. IgA nephropathy
5. Collagen vascular diseases:
• Systemic lupus erythematosus
• Henoch-Schönlein purpura
• Polyarteritis nodosa

PATHOGENESIS
APGN is mediated by immune complexes. Complement activation occurs
primarily through alternative pathway.
168 Selected Topics in Pediatrics for Practitioners

CLINICAL FEATURES
Age group Can occur in any age group. Commonly 5-10 years age group;
males affected more.
• Clinical features depending on degree of renal involvement
• In mild involvement, only asymptomatic microscopic hematuria
• As renal involvement becomes more, varying degrees of other
symptoms:
— Hematuria (urine smoky or reddish)
— Oedema (salt and water retention)
— Hypertension (in about 70% of AGN children)
— Oliguria.
• In severe involvement, presentation like acute renal failure (ARF);
transient ARF is seen in nearly 50 percent of the children with AGN
• Congestive heart failure: Due to salt and water retention and
hypertension
• Encephalopathy: Due to hypertension
— Headache, vomiting, blurred vision
— Alteration in consciousness
— Convulsions
• Ninety percent of the AGN children have the classical nephritis like
presentation.
• The child recovers clinically by two weeks but microscopic hematuria
may be seen as long as one year.

LAB FINDINGS
1. Urine RBCs, frequently RBC casts, WBCs, mild proteinuria of 1+ to
2+
2. Evidence of recent streptococcal infection
a. ASO titre not useful as it may not rise after skin infection
b. Anti DNAse B titre most useful
c. Streptozyme test: Detects antibodies to multiple antigens; this is
also useful
d. Throat culture: May not be useful because of the time interval (2-
3 weeks) between the onset of infection and the onset of APGN.
3. Complements Total hemolytic complements and C3 level are decreased.
4. Kidney biopsy indicated in atypical presentation—presenting as ARF,
nephrotic syndrome, absence of C3, presence of marked hematuria
and/or proteinuria one month after AGN, persistent decreased renal
function, presence of systemic manifestations such as persistent fever,
skin rash, arthritis and hepatosplenomegaly.
 Acute Nephritis and Nephrotic Syndrome 169

COMPLICATIONS
1. Acute renal failure
2. Increased volume overload; heart failure
3. Hypertension
4. Hyperkalemia
5. Acidosis
6. Seizures

PROGRESS
• Starts passing urine well in 4-7 days after onset in majority
• Some may have complications like hypertensive encephalopathy and
CCF; they also usually resolve
• Prolonged oliguria and renal insufficiency in < 5 percent of APGN
children.

TREATMENT
• Supportive measures
• Salt and water retention
• Ten days course of penicillin oral or parenteral
• circulatory congestion:
— O2
— Propped up position
— IV frusemide
— Monitoring
• Hypertension:
— Diuretics (frusemide)
— Calcium channel blockers (nifedepine orally 0.25-0.5 mg/kg
6 hourly).
— Vasodilators (hydralazine)
— ACE inhibitors (enalapril)
• Diet:
— Give liberal calories. If blood urea is normal, give normal protein;
if ARF present, 0.5 to 1.25 g/kg/day protein.
— Restrict sodium during oliguric period; gradually increase during
diuresis.
— Potassium and fruits avoided during oliguric phase.

NEPHROTIC SYNDROME
Nephrotic syndrome (NS) is characterized by:
• Proteinuria (> 40 mg/m2 body surface area/hour)
• Hypoproteinemia (serum albumin < 2.5g/dl)
• Oedema
• Hyperlipidemia
170 Selected Topics in Pediatrics for Practitioners

Proteinuria is the basic feature of nephrotic syndrome leading onto

various other clinical manifestations. In about 90 percent of children
with nephrotic syndrome , it is a primary glomerular problem without
any identifiable disease or cause (idiopathic nephritic syndrome ). Of
these nearly 85 percent belong to minimal change nephrotic syndrome
(MCNS) where there is only insignificant change in renal histology and
good response to corticosteroids. Focal sclerosis(10%) and mesangial
proliferation (5%) are the other types seen among children with idiopathic
nephritic syndrome.
In the remaining 10 percent of nephrotic syndrome, some underlying
conditions may be identifiable such as systemic lupus erythematosus
(SLE) , Henoch-Schönlein purpura and hepatitis B infection.

Minimal Change Nephrotic Syndrome (MCNS)

• This accounts for nearly 85 percent of childhood NS
• Common age group 2 to 6 years; if it occurs in younger(< 1 year) or
older (> 8 years) children, increased likelihood of a significant
glomerular lesion
• More common in boys (2:1 ratio)
• Onset is insidious with oedema noted around eyes and face initially,
followed by oedema of legs and abdomen. If untreated, oedema
becomes generalised and massive with ascites and pleural effusion
and decreasing urine output
• There may be anorexia and abdominal pain
• Some children may have associated respiratory tract and urinary
infections
• Hypertension is uncommon.
• Occasionally a combined nephritic-nephrotic clinical presentation may
be seen with acute onset of oedema, hematuria and massive
proteinuria.

Diagnosis
1. Clinical features
2. Urine analysis
Proteinuria Proteinuria 3+ and 4+; 24 hours urine protein > 2 gm or
> 40 mg/m2/hour; protein: creatinine ratio of > 3
3. Blood
• Serum albumin < 2.5g/dl
• Serum cholesterol (> 250 mg/dl); triglycerides increased
• Renal function (urea, creatinine) normal
4. Renal biopsy Not required in typical cases of MCNS
 Acute Nephritis and Nephrotic Syndrome 171

5. Associated infections Urine culture to rule out urinary tract infection

and tests to rule out tuberculosis (Mantoux test, chest X-ray) are
carried out before steroid therapy.

Complications
1. Infections Children with NS are prone to bacterial infections due to
urinary loss of immunoglobulins, immunosuppressive therapy and
oedema. Spontaneous bacterial peritonitis is the most common serious
infection. Sepsis, pneumonia and urinary tract infection also may
occur. The organisms responsible in most of these infections are
S.pneumoniae and gram-negative bacteria such as E. coli. Tuberculosis
also can occur more frequently in view of prolonged steroid therapy.
Varicella infection can be more severe in children with NS.
2. Coagulation abnormalities Increased tendency for arterial and venous
thrombosis is seen in NS. This hypercoagulable state is due to an
increase in platelet aggregation and hepatic synthesis of clotting factors
and urinary loss of inhibitors of clotting. Renal vein thrombosis is the
commonest presentation.
3. Glomerular sclerosis Persistent proteinuria can cause tubular and
interstitial renal damage resulting in glomerulosclerosis. Hence it is
important to reduce proteinuria by early identification and treatment.

Management
Minimal change nephrotic syndrome in childhood is characterised by
remission and relapses. It is important to counsel the parents about the
need for long-term and repeated treatment.
1. Supportive therapy When oedema is present, no extra salt and normal
fluid intake is recommended unless the oedema is severe. Mild diuretic
such as spironolactone may be used. In severe oedema, IV furosemide
1mg/kg loading dose followed by 1 mg/kg/hr as infusion for a
short period can be used. Twenty-five percent human albumin also
may be used for severe oedema.
2. Specific therapy-prednisolone.

Initial episode Prednisolone 2 mg/kg body-weight daily in 2-3 divided

doses for 4-6 weeks; thereafter prednisolone is reduced to 1.5mg/kg
given on alternate days as a single morning dose for another 4-6 weeks.
It is stopped abruptly after this. Urine becomes protein-free in majority
of children within two weeks. Most patients with NS suffer from relapses
for several years. Relapse is characterised by recurrence of oedema and
not just proteinuria.
172 Selected Topics in Pediatrics for Practitioners

Treatment of Relapse
Relapse is treated with prednisolone 2 mg/kg/day until urine is protein-
free for 3 consective days; then prednisolone 1.5 mg/kg given in the
morning as a single dose on alternate days for 4 weeks and then abruptly
stopped.
In repeated relapses and appearance of severe steroid toxicity
cyclophosphamide therapy is considered (3mg/kg/day as a single dose
for 12 weeks) along with alternate day prednisolone.
Diet High protein, low salt diet.
Prognosis Most children with NS have repeated relapses. Spontaneous
resolution occurs by the end of second decade.

BIBLIOGRAPHY
1. Bergstein JM. Acute post-streptococcal glomerulonephritis, nephrotic syndrome.
In Behrman RE, Kliegman RM, Jenson HB (Eds): Nelson Textbook of Pediatrics
(16th edn). WB Saunders: PA, 2000.
2. David TJ (Ed). Recent Advances in Pediatrics. Churchill Livingstone: London
19:2001.
3. Nammalwar BR, Vasanthi T. Acute Glomerulonephritis. In Parthasarathy A
(Ed): IAP Textbook of Pediatrics (2nd edn). Jaypee Brothers Medical Publishers:
New Delhi, 2002.
4. Srivatsava RN, Bagga A. Nephrotic syndrome. In Parthasarathy A (Ed): IAP
Textbook of Pediatrics. (2nd edn). Jaypee Brothers Medical Publishers: New
Delhi, 2002.
 18
Management of Common
Endocrine Problems:
Current Concepts
P Venkataraman, PG Sundararaman

CONGENITAL HYPOTHYROIDISM
• Diagnosis and treatment of congenital hypothyroidism is a medical
emergency and on clinical suspicion blood sample should be sent for
hormonal assays and specific therapy must be started at the earliest,
based on clinical and hormonal study (taking into consideration the
variation in thyroid hormone in newborn).
• Replacement therapy with sodium levothyroxin (Na L T4) should be
started when the hypothyroidism is proved. What is much more
important is that the parents of these children should be counselled
regarding the causes of congenital hypothyroidism, much more
important is that they should understand the importance of
compliance and the excellent prognosis in most babies if therapy is
initiated sufficiently early and is adequate. They must be explained
the importance of life-long therapy of this disorder in majority of this
population.
• The prime aim should be to normalize the serum T4 level as early
as possible and an initial dosage of 10-15 mic g/kg is recommended
so as to achieve this end.
• Babies with compensated hypothyroidism may be started on the
lower dosage, while those with severe congenital hypothyroidism
such as those with thyroid agenesis should be started on the higher
dosage.
• Thyroid hormone may be crushed and administered with water or
milk, but care should be taken that the medicine is swallowed as a
whole without any pilferage. Care must be taken not to mix thyroxin
with substances that interfere with its absorption, such as iron, soy,
or fiber.
174 Selected Topics in Pediatrics for Practitioners

• Thyroxine is available only as a tablet form of 25, 50 and 100 micgm

and the liquid preparations are unstable and should not be made to
dispense.

Aims of Therapy
• Normalize T4 as soon as possible
• Avoid hyperthyroidism to manifest overtly
• Promote normal growth and development
• When levothyroxine is used in the appropriate formula and in
adequate dosage, one can anticipate the T4 to normalize in most
infants within 1 week and the TSH within 1 month. Further
adjustments in the thyroxin dosage are made according to the results
of thyroid function tests (TFT) clinical picture and weight of the
child. Often small increments or decrements of L-thyroxine (12.5 μg)
are needed.
• Some infants will develop supra physiologic serum T4 values on this
amount of thyroid replacement but the serum T3 concentration usually
remains normal, affected infants are not symptomatic, and available
information suggests that these short-term T4 elevations are not
associated with any adverse effects on growth, bony maturation, or
cognitive development.
• In rare infants, normalization of the TSH concentration may be delayed
because of relative pituitary resistance. In such cases, FT4 will be a
better index to assess and monitor.
• The treating clinician should aim at keeping the level of T4 always
at the upper limit of normal and that of TSH within normal limits.
• Recommended protocol for monitoring these children:
• Repeat T4 and TSH at 2 and 4 weeks after the initiation of Na L T4
treatment,
• Every 1-2 months during the first year of life,
• Every 2-3 months between 1 and 3 years of age,
• Every 3-12 months thereafter until growth is complete.2

Suspected Cases of Transient Hypothyroidism

In all these children temporarily wean them from thyroxine for a short
while, i.e. 6 to 8 weeks, of course after the age of 3 years when most
thyroxine-dependent brain maturation has occurred and repeat FT4 and
TSH, if it is normal repeat after 3 months and if it is abnormal reinstate
the same dose and larthyroxine.

Whether to Treat Preterm Babies?

It seems reasonable at the present time to treat any premature infant
with a low T4 and elevated TSH and to consider treatment of any infant
 Management of Common Endocrine Problems: Current Concepts 175

< 27 weeks with a low T4 whether or not the TSH is elevated. A dosage
of 8 micgm/kg/day in the latter group of infants is recommended.

Risk Factors for Poor Prognosis

• Most severe in utero hypothyroidism as determined by initial T4
level and much poor skeletal maturation at birth are likely to have
permanent intellectual sequelae. This has led to the conclusion that
some cognitive deficits in the most severely affected babies might not
be reversible by postnatal therapy.
• When a higher initial treatment dose is used like 10 to 15 μgm/kg
and treatment is initiated earlier before 2 weeks of age this
“development gap” can be closed, irrespective of the severity of the
congenital hypothyroidism at birth3
• According to a study by Bongers-Schokking et al, even babies with
severe congenital hypothyroidism can achieve normal psychomotor
development at 10 to 30 months as long as treatment is initiated
before 13 days of age and an initial dose of > 9.5 μgm/kg/day is
used. However, if treatment is delayed or a lower dose is used, a 20
point deficit in both mental and psychomotor development is
observed4
• In addition to adequate dosage, good compliance is also a very
essential prerequisite for an optimal developmental outcome.
Importance of earlier identification and initiation of treatment
• Unfortunately, only 10 percent of affected infants were diagnosed
clinically within the first month of life and only 35 percent within the
first 3 months of life . and hence the need for a neonatal screening
programme5
Justification for neonatal screening for CH
• A common disorder, 4-5 times more common than phenylketonuria
for which screening program is already in vogue.
• Treatable cause of mental retardation and hence the diagnosis must
be made early, preferably within the first few days of life.
• Clinical recognition is difficult if not impossible at that sensitive
vulnerable age.4
• Available specific screening tests are sensitive and reprodusable.
• If diagnosed earlier, treatment is simple, cheap and effective and
available everywhere.
• Highly favorable cost benefit ratio.
• The first pilot screening program for the detection of congenital
hypothyroidism was established in Quebec in 1972. Eventhough there
seems to be some controversy, evidence suggests that a normal
outcome is possible if treatment is started aggressively, adequately
and sufficiently early.
176 Selected Topics in Pediatrics for Practitioners

Main Objective of Screening

1. Eradication of mental subnormality due to hypothyroidism.
2. Incidentally, evaluation of the prevalence of the various causes of
congenital hypothyroidism, including a series of transient disorders
seen predominantly in premature infants.

AUTOIMMUNE THYROIDITIS (HASHIMOTO’S THYROIDITIS)

Hashimoto’s thyroiditis is characterized clinically by:
• Painless, diffuse enlargement of the thyroid gland.
• Classically firm in consistency.
• Girl children are more affected than boys.
• In some cases there is a propensity to inherit as autosomal dominant
with female sex predominance.
• Affects children between 4 to 10 years more commonly.
• Common cause of thyromegaly in iodine sufficient areas.
• Most of the children are euthyroid and eumetabolic but hypothyroi-
dism may develop.
• Histologically, thyroid parenchyma is diffusely replaced by a
lymphocytic infiltrate and fibrotic reaction; frequently, lymphoid
germinal follicles are visible.
• Afflicted children with Hashimoto’s thyroiditis have serum antibodies
reacting with thyroglobulin, thyroidperoxidase, and against an
unidentified protein present in colloid. In addition, many patients
have cell mediated immunity directed against thyroid antigens,
demonstrable by several techniques.
• Review of literature also emphasizes a basic abnormality in the
immune surveillance system, which in some way allows auto-
immunity to develop against thyroid antigens, and as well against
other tissues, including stomach, adrenal, and ovaries, in many
patients with thyroiditis.
• This response may include cytotoxic antibodies, stimulatory anti-
bodies, blocking antibodies, or cell mediated immunity. Thyrotoxicosis
is viewed as an expression of the effect of circulating thyroid
stimulatory antibodies.
Hashimoto’s thyroiditis is predominantly the clinical expression
of cell mediated immunity leading to destruction of thyroid cells,
which in its severest form produces thyroid failure and idiopathic
myxedema in adults.
• The thyroid gland tends to lose its ability to store iodine, produces
and secretes iodoproteins that circulate in plasma, and is inefficient
in making thyroxine hormone. Thus, the thyroid gland is under
increased TSH stimulation, fails to respond to exogenous TSH, and
has a rapid turnover of thyroidal iodine.
 Management of Common Endocrine Problems: Current Concepts 177

• Gold standards for diagnosing this condition is positive titers of TG

Ab and/or TPO Ab and the characteristic finding in FNAC thyroid,
with the child in euthyroid or hypothyroid status.

Management Protocol
• Small goiter with clinical euthyroidism does not require therapy
unless the TSH level is elevated.
• Indications for Na L T4:
1. Large gland leading on to cosmetic insult
2. Progressive growth of the goiter
3. Associated hypothyroidism
• Surgery is seldom indicated.
• Experience in our pediatric endocrine OPD is that even in young
patients the response to therapy takes a somewhat longer time and
is mandatory on the part of the treating physician to explain this
important aspect to the parents. There is no evidence that thyroid
replacement actually halts the ongoing process of thyroiditis, but in
some patients receiving treatment, antibody levels gradually fall over
many years.
• Therapy is probably indicated if the TSH level is elevated and the
FT4 is low normal, since the onset of hypothyroidism is predictable
in such patients.
• The dosage of thyroxine should normally be that required to bring
the serum TSH level to the low normal range,which is achieved with
2-4 μgm/kg body weight/day.
• Once thyroxine treatment is initiated, it is required to be continued
for a longer period, of course with periodical monitoring of clinical,
biochemical, radiological and serological parameters.
• However, it has been found that up to 20 percent of initially hypo-
thyroid individuals will later recover and have normal thyroid
function if challenged by replacement hormone withdrawal. This
may represent subsidence of cytotoxic antibodies, modulation of
TSBAb, or some other mechanism.
What is the role of prophylactic hormonal replacement therapy?
• The problem of autoimmunity is an ongoing process and Hashimoto’s
thyroiditis develops into hypothyroidism at any time during the
course of disease process . Clinical trials with proplylactic thyroxine
in a dose of 1.0 ~ 2.0µg/kg/day for one year in euthyroid patients
with Hashimoto’s thyroiditis showed decrease of anti-TPO antibodies
and thyroid B-lymphocytes, suggesting prophylactic T4 therapy might
be useful to prevent progression of disease to some extent.
178 Selected Topics in Pediatrics for Practitioners

Role of Steroids?
• There are instances wherein glucocorticoid therapy was started during
the onset of goiter when associated with pain which has alleviated
the symptoms and improved the associated biochemical
abnormalities.
• Some studies have shown steroid therapy to increase plasma T3 and
T4 levels by suppression of the autoimmune process.7
• Blizzard and co-workers8 have given steroids over several months to
children in an attempt to suppress antibody production and possibly
to achieve a permanent remission. The adrenocortical hormones
dramatically depress clinical activity of the disease and antibody
titers, but all return to pretreatment levels when treatment is
withdrawn and hence it is concluded not to venture with steroids
because of the undesirable side effects of the drug.
• Chloroquine has been reported in one study to reduce antibody titers7
but was not in vogue because of its toxic effects.

CENTRAL PRECOCIOUS PUBERTY (CPP) (GnRH DEPENDENT):

BASIC PRINCIPLES OF TREATMENT
1. To halt and/or to reverse sexual development
2. To recess the rapid growth which could otherwise lead on to short
adult stature.
This could be achieved by way of either treating the underlying
condition or by changing the hormonal balance in the body to stop
sexual development. It becomes impracticable often to treat the
underlying conditions, as some of them are idiopathic. Some CNS tumors
whose only manifestation is precocious puberty often do not require
surgical management. Treatment therefore is aimed at changing the
hormonal balance in the system.

Medroxyprogesterone Acetate (MPA)

This drug was used unsuccessfully , until three decades ago. MPA stops
menstruation, may or may not reduce the breast size and fails to stop
rapid growth in either sex and ineffective on sexual development in
boys. Side effects associated with the use of MPA are related to its
structural similarity to glucocorticoids, with long-term use it may cause
adrenal suppression and in higher dosage cushingoid features.

GnRH or LH-RH Agonists

These are a group of synthetic analogues of the amino acid sequence of
the natural LH-RH decapeptide and are the treatment of choice for
 Management of Common Endocrine Problems: Current Concepts 179

central precocious puberty (CPP), whether idiopathic or orga-

nic.Treatment with these long acting GnRH-A has revolutionized the
management of CPP.
Their role in regression of features of precocious puberty and
secondary sexual characters is well established. Long acting GnRH-A
therapy is effective in improving the auxological outcome of patients
with CPP. Maximum benefit is observed in girls with greater bone age
advancement at a younger age and for a longer duration of treatment.
Small changes in the GnRH molecule have longer, beneficial clinical
effects. GnRH-A become much more resistant to enzymatic degradation,
has got more affinity for the receptor on the pituitary gonad trope,
increased hydrophobicity and with some analogues, increased binding
to plasma protein. The super active agonist analogues of GnRH have
about 15-200 times the potency of natural GnRH decapeptide, prolonged
action and minimal toxicity.
Natural GnRH is released in pulses, leading on to pulsatile release
of gonadotropins, but continuous GnRH administration decreases
gonadotropin secretion. Paradoxically GnRH-A first stimulate and then
in a few days, suppress pulsatile LH and FSH release, gonadal steroid
output and gametogenesis. Suppression initially is from down regulation
and loss of receptors but later receptor levels return to normal and
desensitization persists because of uncoupling of the receptors from the
intracellular signaling effector pathway. GnRH-A has got the distinction
of selectively suppressing the gonadotropins without interfering directly
with release of the other pituitary hormones. In essence , the regimen
induces a reversible medical gonadectomy.
GnRH-A available for the pharmacologic treatment of CPP include:

Leuprolide Acetate
• Available in a monthly depot formulation for intramuscular use.
Initial dose: 300 μgm/kg/month, standard package include 3.5 μgm,
7.5 μgm vials.
• Dosage for subcutaneous preparation is 20-50 μcg/kg/day. Toxic
effects include hypersensitivity and pernicious anemia. Approximately
5 percent of children develop an immune response to the
encapsulation material of depot preparation.
• Discontinue depot preparation if sterile abscess forms at the injection
site and/or systemic symptoms develop, including fever and chills.
• Daily S/C preparation may be substituted by another preparation .
Nafarelin
• A decapeptide synthetic analogue which can be administered
intranasally also. It is considered as second line agent if Leuprolide
proves difficult to administer.
180 Selected Topics in Pediatrics for Practitioners

• Dose 800-1600 μgm/day intranasal, administered as two sprays in

each nostril, twice a day.
• Dosage for subcutaneous preparation is 4 μg/kg/day.

Deslorelin
Subcutaneous/Depot intramuscular—4-8 μg/kg/day.

Tryptorelin
Available both for subcutaneous(20-40 μgm/kg/day) and intramuscular
depot preparation (60 μgm/kg/month)

Buserelin
• Subcutaneous 20-40 μgm/kg/day
• Intranasal 1200-1800/μgm/kg/day.

Histerelin
Subcutaneous 8-10 μgm/kg/day.
The effectiveness of LHRH-A is a function of the potency of the
analogue, dose, route of administration and compliance and for
evaluating the effectiveness periodical monitoring of clinical , radiological
and hormonal parameters is mandatory. Poor compliance, on the part
of the patient, irregular treatment or inadequate dosage results in
persistent or intermittent increase in the serum level of gonadal steroids
and may lead on to continued advancement of bone age.

How to monitor these Children?

• Serial measurement of growth, staging of secondary sexual characters,
bone age and in girls serial pelvic ultrasonographic evaluation of
uterine size and ovarian morphology is essential.
• A decrease in the uterine and ovarian size predicts better outcome.
• Hormonal monitoring includes, periodic determinations of
testosterone levels in boys, estradiol levels in girls and the LH response
to exogenous GnRH or basal gonadotropin levels.
• Prepubertal estradiol and testosterone indicates adequate gonadal
suppression.
• Girls experience a reduction in the breast size and amount of public
hair, stoppage of menses if present already, within the first 6 months
of therapy and concomitant pelvic ultrasonogram indicates reduction
in uterine and ovarian size.
• In boys, testicular volume diminishes, there will be thinning of pubic
hair, regression of acne and seborrhoea, masturbation and penile
 Management of Common Endocrine Problems: Current Concepts 181

erections becomes less frequent and the self esteem improves with
reduction in high energy level and aggressive behavior.
• The elevated growth hormone level in CPP also results in a decrease
with GnRH- A treatment, more so during sleep and to provocation
stimuli. Children with CPP have higher mean serum IGF-1 for chrono-
logical age, similar to the classical elevated IGF-1 levels of normal
puberty. GnRH-A treatment reduces the level of IGF-1 to the normal
range for bone age but not for chronological age coupling growth
hormone therapy with GnRH-A will benefit the final adult stature.
There will be normal resumption of pubertal activity after disconti-
nuation of GnRH-A treatment indicating that there is no dealy in the
development of hypothalamo pituitary axis in girls with CPP who are
treated with GnRH-A. Before beginning treatment it is essential to
establish the progressive nature of the sexual precocity because these
drugs are much more effective in most severely affected girls with rapidly
progressive sexual precosity.

CONGENITAL ADRENAL HYPERPLASIA (CAH)

Classic, Salt Wasting Type of
21-Hydroxylase Deficiency (21-OH D-CAH)
Electrolyte abnormalities generally take from a few days to 3 weeks to
appear because the placenta maintains the fetal electrolytes in utero. In
mild forms of salt-wasting adrenal hyperplasia, salt wasting may not
become apparent until the child is stressed by an illness.

How to Stabilise the Neonate ?

Kindly look for life-threatening complications like:
1. Dehydration
2. Hypoglycemia
3. Dyselectrolytemia
4. Hypotension
5. Vascular collapse
6. Cardiac arrest
• Give intravenous bolus of isotonic sodium chloride solution 20 mL/
kg over the first hour as needed to restore intravascular volume and
blood pressure.
• This dosage may be repeated if the blood pressure remains low.
• It should be followed by a continuous IV infusion of isotonic sodium
chloride solution or half isotonic sodium chloride solution to restore
intravascular volume.
• Dextrose must also be provided. If the patient is hypoglycemic, 2-4
mL of dextrose 10 percent in water (D10W) corrects the hypoglycemia.
182 Selected Topics in Pediatrics for Practitioners

Dextrose 5 percent in water (D5W) must be provided to prevent

further hypoglycemia or prevent hypoglycemia from occurring if the
patient is not hypoglycemic.
The frequency, amount and type of intravenous fluid are adjusted
depending upon the clinical status, status of dehydration, body weight,
serum electrolytes, and blood pressure.
On clinical suspicion when the provisional diagnosis is made, we
used to send blood samples for electrolytes, blood sugar, cortisol,
aldosterone, and 17-hydroxyprogesterone concentrations, and the patient
is treated with specific glucocorticoids therapy pending lab reports,
because this may be life preserving .

Specific Steroidal Replacement Therapy

should be Started Simultaneously
• Give injection hydrocortisone 50-100 mg/m2 or 1-2 mg/kg IV as an
initial dose followed by 50-100 mg/m2/d IV divided q6
• Methylprednisolone and dexamethasone have negligible
mineralocorticoid effects; thus, if the patient is hypovolemic, hypo-
natremic, or hyperkalemic, large doses of hydrocortisone (double or
triple the stress doses mentioned above) are preferred.
• Currently, no parenteral form of mineralocorticoid is available , but
if the patient has good GI function, administer Tab fludrocortisone
0.1-0.2 mg per oral/per day.
After stabilising the neonate start long-term medical therapy and
Kindly remember the treatment is for Life long !!

Goal of Therapy
• Replacement of glucocorticoid and mineralocorticoid to prevent signs
of adrenal insufficiency
• To prevent the accumulation of precursor hormones that cause
virilization.
Remember the prefered steroid is a combination of hydrocortisone
and fludrocortisone, but in our practice cost of these drugs is a real
problem faced by most of our parents.
• Hydrocortisone is available in tablets of 5, 10, and 20 mg. Hydro-
cortisone is recommended in the pediatric population because of its
lower potency that permits easier titration of appropriate doses and
this is the physiological steroid.
• Tab fludrocortisone 0.05-0.2 mg/d per oral to all these children.
 Management of Common Endocrine Problems: Current Concepts 183

Long-term Medical Therapy

• The goal of therapy of adrenal hyperplasia is the replacement of
glucocorticoid and mineralocorticoid to prevent signs of adrenal
insufficiency and to prevent the accumulation of precursor hormones
that cause virilization.
• Adequate glucocorticoid replacement should prevent excessive-
concentrations of ACTH from stimulating the adrenal glands to
produce abnormal concentrations of adrenal androgens that result in
further virilization.
• In the growing child with adrenal insufficiency, long-term gluco-
corticoid replacement must be balanced to prevent symptoms of
adrenal insufficiency while still allowing the child to grow at a normal
rate and prevent symptoms of glucocorticoid excess.
• Dosage must be tailored to each patient, but the general average
dose is in the range of 10-25 mg/m2/d per oral of hydrocortisone
divided in 2-3 doses.
Prednisone, prednisolone, or even dexamethasone may be used. The
estimated equivalencies are:
1 mg prednisone = 4 mg hydrocortisone
1 mg prednisolone = 5 mg hydrocortisone
1 mg dexamethasone = 50 mg hydrocortisone
These forms of glucocorticoid have the advantage of having longer
half-lives than hydrocortisone and, therefore, require twice-a-day dosing
or even once-a-day dosing (dexamethasone), which often aids
compliance. However, because of the increased potency, growth
suppression and other signs of glucocorticoid excess are common.
• Administer fludrocortisone 0.05-0.2 mg/d per oral to patients with
mineralocorticoid deficiency. Adjust the dose based on PRA (plasma
renin activity).
• Administer 2-5 g/d NaCl to infants to counteract salt wasting. Older
children can usually scavenge adequate salt to provide for their needs
and may lose their salt-wasting tendencies as they mature.
• The dose of glucocorticoid is adjusted clinically (absence of symptoms
of glucocorticoid deficiency and normal growth) and by periodically
measuring the concentrations of precursor hormones.

How to Monitor these Children?

Monitor them clinically, anthropometrically, biochemically, radiologically
and hormonally.
• Clinically, monitor the growth pattern, height and weight percentile,
look for signs of steroid over dosage, monitor blood pressure, adjust
dosage during stress and intercurrent illnesses but never stop steroid.
184 Selected Topics in Pediatrics for Practitioners

• The dose of glucocorticoid is adjusted clinically (absence of symptoms

of glucocorticoid deficiency and normal growth) and by periodically
measuring the concentrations of precursor hormones. For example,
in 21-hydroxylase deficiency, keeping plasma concentrations of 17-
hydroxyprogesterone in the 200-500 ng/dL range and andro-
stenedione in the normal physiologic range is desirable.
• Plasma ACTH concentrations are of little help in adjusting doses of
glucocorticoid for patients with primary adrenal insufficiency.
Symptoms of salt craving, blood pressure, PRA, and electrolytes are
helpful in adjusting the dose of fludrocortisone. High blood pressure
with suppressed PRA should prompt a reduction in fludrocortisone
dose.

What to do During Stress?

• In the patient with a minor illness (temperature < 38°C), the dose of
hydrocortisone should be at least doubled.
• For patients with more severe illness (temperature >38°C), the dose
of glucocorticoid should be tripled.
• If the patient is vomiting or listless, administer parenteral
glucocorticoid (hydrocortisone 50-75 mg/m2 IM/IV. Because hydro-
cortisone succinate has a short duration of action, the dose must be
repeated every 6-8 hours at a daily dose of 50-100 mg/m2/d until the
patient is well.
What is New in the Management Protocol?
Combination of glucocorticoid (to suppress ACTH and adrenal androgen
production), mineralocorticoid (to reduce angiotensin II concentrations),
aromatase inhibitor (to slow skeletal maturation), and flutamide (an
androgen blocker to reduce virilization).

When to Refer this Virilized Female Child to a Pediatric Surgeon?

• The traditional approach to the female with ambiguous genitalia due
to adrenal hyperplasia is clitoral recession early in life, followed by
vaginoplasty after puberty.
• Some female infants with adrenal hyperplasia are only mildly virilized
and may not require corrective surgery if they receive adequate
medical therapy to prevent further virilization.
• Literature reviews suggest bilateral adrenalectomies in the manage-
ment of virilizing forms of adrenal hyperplasia in order to prevent
further virilization and advancement of skeletal maturation.

Any Special Diet for these Infants?

Patients should have ample access to salt and supplement these infants
who have salt wasting with 2-4 g of NaCl per day added to their formula.
 Management of Common Endocrine Problems: Current Concepts 185

Caloric intake may need to be monitored and restricted if excess

weight gain occurs because glucocorticoids stimulate appetite.

SHORT STATURE DUE TO GROWTH

HORMONE DEFICIENCY (GHD)
The Final Diagnosis of GH Deficiency is Based on
1. Clinical
2. Auxological (growth)
3. Biochemical data.

Suspect GHD
1. If a child has reduced height velocity
2. Delayed bone age
3. Low serum levels of the GH surrogates, insulin-like growth factor-
1 (IGF-1), and insulin-like binding protein-3 (IGFBP-3) not otherwise
explained by young age and/or undernutrition.
4. Low serum GH levels
• kindly note that beyond the first month of life, measurement of
GH levels in a random blood sample is without value to make a
diagnosis of GH deficiency because most of the body’s GH is
made during sleep, with several significant peaks linked to deep
(stage III-IV EEG) sleep, the first cycle of which usually occurs at
approximately 60 to 90 minutes after falling sleep.
• GH testing is then recommended by any of several physiologic or
pharmacologic methods. The most commonly employed
physiologic stimulus is exercise, but this is often difficult to
standardize. Overnight serial blood sampling every 20 to 30
minutes was common in the early 1990s but lost favor because of
inconvenience, cost, and lack of reproducibility.
• A more common approach is growth hormone dynamic testing
(provocative testing) with medications known to activate the
physiologic regulation of GH secretion, notably the α-adrenergic
pathway (e.g., clonidine at a dose of 4 μgm/kg, each tablet available
as 100 micgm strength).
• Blood samples are sent for GH assay at fasting, 60 and 90 minutes
after the clonidine is taken. Clonidine may cause sleepiness,
hypoglycaemia and a mild fall in blood pressure, but these effects
are transient and usually resolve within 90 minutes.
• These and all other stimulation tests must be performed in the
fasting state early in the morning, as glucose intake suppresses
GH secretion.
186 Selected Topics in Pediatrics for Practitioners

• GH provocation tests can also be performed using glucagon (0.1

mg/kg, maximum dose 1 mg) or insulin (0.05 to 0.1 units of
regular insulin per kilogram, depending on the index of suspicion),
the latter known as an insulin tolerance test (ITT).In both cases,
hypoglycemia is induced. In the case of glucagon, blood sugar
initially rises followed by stimulation of endogenous insulin
leading to late hypoglycemia.
• For a hypoglycemic stimulus to be deemed adequate to stimulate
GH, the plasma glucose concentration needs to fall by at least 50
percent from baseline. In the glucagon test, blood sampling is
performed every 15 minutes for 1 hour and then every 30 minutes
for the next 2 hours out to 180 minutes. For the ITT, blood sampling
is performed every 15 minutes for 1 hour and then again 30
minutes later, with bedside and laboratory glucose testing, along
with GH measurements at all time points and cortisol
measurements at 0, 60, and 90 minutes. To obtain these multiple
blood samples, a heparin lock should be placed in a large-bore
vein at the start of the study. Glucagon or hypoglycemia itself
may cause nausea and vomiting. Hypoglycemia results in
uncomfortable adrenergic manifestations such as sweatiness,
excessive hunger, and shakiness, and may also cause
neuroglycopenic manifestations such as loss of consciousness or
seizures.
• It is to be kept in mind that these tests are moderately dangerous
and need to be performed by experienced personnel as inpatient
with resuscitative equipment and expertise as well as with a
physician in attendance throughout the test. If dangerous
hypoglycemia associated with diminished mental status occurs,
2 mL/kg of 25 percent dextrose should be immediately adminis-
tered intravenously. The test will still be valid because the
hypoglycemic stimulus was delivered so all blood samples should
continue to be collected.
• Arginine is another GH secretagogue that requires a 45 minute
intravenous infusion (5 mL/kg of 10% arginine hydrochloride).
Arginine is an amino acid that is a nonspecific stimulator of
multiple hormones including insulin and glucagon, in addition to
GH. There are no side effects with its use.
• Lastly, intravenous GH-RH (at a dose of 1 µg/kg body weight)
may be employed with sampling at 0, 5, 30, 45, 60, 90, and 120
minutes.Its only frequent side effects are local injection site
reactions. In younger infants instead of dynamic study—a
deficiency in blood glucose less than 50 mg% by delaying the
feeds is matched with growth hormone sampling.
 Management of Common Endocrine Problems: Current Concepts 187

GH deficiency is traditionally defined by all GH levels on all tests

being less than 10 ng/mL as measured by traditional double-antibody
radioimmunoassay.
• Once the diagnosis of hypopituitarism has been made by
appropriate hormonal testing, a MRI brain scan with gadolinium
contrast must be performed to look for a possible organic or
structural basis. Abnormalities with hypopituitarism include a
small pituitary gland with filling of the sella with cerebrospinal
fluid (empty sella) and an ectopic posterior pituitary gland. A
midline syndrome is suggested by the absence of the septum
pellucidum and/or the corpus callosum.
• The most critical reason for obtaining the MRI scan is to detect
a brain tumor in the hypothalamic-pituitary area, the most
common of which is a craniopharyngioma.
• Radiological evidence of craniopharyngiomas can be seen on a
lateral skull-ray in 89 percent of cases, which makes this an
important screening test when this diagnosis is suspected in a
child. Findings include erosion of the normal sellar architecture
and/or the presence of suprasellar calcification.
• On MRI scans, the tumor usually contains a mixture of solid and
cystic components and may contain a ring of calcification around
a cystic component (the latter best seen on a computed
tomographic scan). Other abnormalities that can be seen on the
MRI scan include a transected stalk, small optic nerves, hydro-
cephalus, and vascular abnormalities.
• If an underlying cause is discovered on the MRI of the head, such
as a tumor and/or hydrocephalus, appropriate neurosurgical
intervention is required. For example, removal or debulking of a
tumor and shunting for hydrocephalus, respectively, would be
undertaken. Additionally, radiation therapy may be required to
treat certain types of tumors. Chemotherapy is used less often to
treat brain tumors. In most cases, these treatments, while poten-
tially life-saving, do not reverse the hypopituitarism.

Growth Hormone Therapy

• GH manufactured by DNA recombinant technology, available both
as a lyophilized powder and liquid form is given subcutaneously
either with a 31-gauge needle and syringe, pen system with a 31-
gauge needle, or “needleless” injector system. The usual dose range
is between 0.18 and 0.3 mg per kilogram of body weight per week
or 0.65 to 1.77 mg/m2/day divided into 6 or 7 daily doses adminis-
tered generally in the evening to simulate the fact that most of the
GH manufactured by the body is at night during sleep (nyctohemeral
188 Selected Topics in Pediatrics for Practitioners

rhythm). Associated hyothyroidism will blunt the response of GH

therapy and hence it has to be investigated and treated first.
• If the hypopituitarism is caused by a brain tumor or its treatment,
commencement of GH treatment is usually delayed for 1 year until
the clinical status of the tumor is clearly defined. This practice is
based on logic because there are no scientific data showing that GH
causes tumor growth or recurrence. Longer acting growth hormone
and growth stereognosis are to be put in clinical practice in future.

REFERENCES
1. New England Congenital Hypothyroid Collaborative: Correlation of cognitive
test scores and adequacy of treatment in adolescents with congenital
hypothyroidism. J Pediatr 1994;124:383.
2. Lafranchi S, Dussault JH, Fisher DA, et al. American Academy of Pediatrics
and American Thyroid Association. Newborn screening for congenital
hypothyroidism: Recommended guidelines. Pediatrics 1993;91:1203.
3. van Wassenaer AG, Kok JH, de Vijlder JJM, et al. Effects of thyroxine
supplementation on neurologic development in infants born at less than 30
weeks’ gestation. N Engl J Med 1997;336:21.
4. Bongers-Schokking JJ, Koot M, Wiersma D, Verkerk PH et al. Influence of
timing and dose of thyroid hormone replacement on development in infants
with congenital hypothyroidism. J Pediatr 2000;136:292.
5. Klein AH, Meltzer S, Kenney FN. Improved prognosis in congenital
hypothyroidism treated before age 3 months. J Pediatr 1972;81:912.
6. Yamada T, Ikejiri K, Kotani M, Kusakabe T. An increase of plasma
triiodothyronine and thyroxine after administration of dexamethasone to
hypothyroid patients with Hashimoto’s thyroiditis. J Clin Endocrinol Metab
1981;46:784.
7. Blizzard RM, Hung M, Chandler RW, Aceto T Jr, Kyle M, Winship T.
Hashimoto’s thyroiditis. Clinical and laboratory response to prolonged cortisone
therapy. N Engl J Med 267:1015.
8. Ito S, Tamura T, Nishikawa M. Effects of desiccated thyroid, prednisolone and
chloroquine on goiter and antibody titer in chronic thyroiditis. Metabolism
1968;17:317.
 19
Recognition and Initial
Management of
Critically Ill Child
P Ramachandran

• How to identify a critically ill child?

• What are the predisposing conditions?
• What is the initial management of critically ill child?
“Critically ill child” means a child who is in a clinical state which
may result in respiratory or cardiac arrest or severe neurologic
complication, if not recognised and treated promptly. This term does not
refer to any particular disease, but many diseases can lead onto “critically
ill state”. Whether a child presents with a primary cardiovascular, respi-
ratory, neurologic, infectious or metabolic disorder, the goal is early
recognition of respiratory and circulatory insufficiency. In clinical practice,
there are three common situations that characterise a critically ill child:
1. Respiratory distress
2. Shock and
3. Altered sensorium .
Early intervention is geared towards preventing the progression of
hypoxemia and hypoperfusion to full cardiorespiratory arrest.
It is easy to recognise a critically ill child when there is an obvious
problem like severe trauma or unconsciousness. On the other hand it is
important to identify a child with physiological derangement in its early
stages when signs are subtle. The “golden hour” concept applies to all
children with illnesses presenting as emergency. Early recognition of a
“critically ill child” requires a systematic and rapid clinical assessment
with a background knowledge of age appropriate physical signs.
There are many methods to assess an acutely ill child. A very simple
and quick way of assessment of overall illness and injury severity is by:
1. Appearance of the child
2. Breathing
3. Circulatory status
190 Selected Topics in Pediatrics for Practitioners

These three parameters comprise “Pediatric assessment triangle”

Appearance Breathing

Circulation

APPEARANCE OF THE CHILD

Appearance basically denotes the neurological status. It is determined
by the oxygen and blood supply to the brain which are dependent on
cardiopulmonary status and the structural integrity of the brain. The
parameters assessed in appearance are alertness, distractibility or
consolability, eye contact, speech or cry, motor activity and color of the
skin. In addition, seizures, abnormal posturing, muscle tone and pupillary
reaction are noted.
1. Alertness Normal children exhibit awareness and interest in
surroundings. Determine if the child is confused, irritable, lethargic
or totally unaware of environment. Changes in level of consciousness
can also be rapidly assessed by AVPU method.
• Awake
• Responsive to voice
• Responsive to pain
• Unresponsive
2. Distractibility or consolability by parent is a normal phenomenon in
infants and young children. Children with serious illness will be
continuously irritable and cannot be consoled.
3. Eye contact with parents or caretaker is noted normally after 2 months
of age. Failure to do this is an early ominous sign of hypoperfusion
or dysfunction of brain. Even a history by mother of not having eye
contact is an important warning sign.
4. Speech/cry Whether the cry is normal or whimpering or moaning or
high pitched. High pitched cry or moaning sounds indicate serious
illness.
5. Motor activity Normal movements of limb, trunk and neck.
6. Colour of the skin denotes respiratory and circulatory status. Skin of
palm and fingers must be pink (normal). Pale, cyanosed, mottled or
ashen grey colour denotes circulatory/respiratory dysfunction.
 Recognition and Initial Management of Critically Ill Child 191

Other Features in Appearance

Seizure activity: Seizures with altered sensorium is a critically ill state
as it may lead onto cardiorespiratory compromise or neurologic sequelae
if not treated.
Posturing Intermittent flexor (decorticate) or extensor (decerebrate)
posturing occurs with prolonged cerebral hypoperfusion.
Muscle tone Hypotonia and limpness may occur in hypoxia, shock or
primary neurologic problem.
Pupil size Pupils may be small but reactive in cerebral hypoperfusion.
Unequal pupils is a medical emergency; may indicate increased
intracranial pressure (ICP) and impending coning.

Breathing
1. Respiratory rate Tachypnoea is an early sign of respiratory distress. A
respiratory rate of more than 50/minute in infant and more than 40/
minute in older children is tachypnoea. Tachypnoea without increased
work of breathing (Quiet tachypnoea) is seen in shock, heart disease
and acidosis. A slow or irregular respiratory rate in an acutely ill
child is ominous.
2. Work of breathing Increased work of breathing (IWB) is recognized by
nasal flaring, grunting, intercostal, subcostal and suprasternal
retractions. Head bobbing and see saw respirations (severe chest
retraction with abdominal distension) are more advanced signs of
respiratory distress and impending respiratory failure.
3. Air entry Effective tidal volume is assessed by good chest expansion
and well heard breath sounds on auscultation.
4. Pulse oximetry Oxygen saturation assessment is an important adjunct
to identify oxygenation state in acutely ill child.

Circulation
Circulation is assessed to find out if the cardiac output meets the tissue
demand. Shock is defined as circulatory dysfunction in which there is
inadequate delivery of oxygen and substrates to meet the metabolic
demands of tissues. Circulatory status is assessed by heart rate, skin
perfusion, systemic perfusion and blood pressure.
1. Heart rate Tachycardia is a common response to a variety of stresses
including shock. Hence its presence mandates further evaluation.
Bradycardia in a critically ill child is ominous.
2. Pulses Simultaneous palpation of central (femoral, carotid and
brachial) and peripheral (radial, dorsalis pedis and posterior tibial)
192 Selected Topics in Pediatrics for Practitioners

pulses is done. In early shock peripheral pulses are weak. Loss of

central pulse is to be treated as cardiac arrest.
3. Skin perfusion
a. Temperature When ambient temperature is warm, hands and feet
should be warm. Hands and feet become cold when cardiac output
falls.
b. Colour Normally the colour is pink over the palms upto the fingers.
Pallor or cyanosis or mottling denote decreased perfusion.
c. Capillary refill time (CRT) Normal is less than 2 seconds. Delayed
CRT is again a feature of early shock. It is looked for by elevating
the limb above heart level; blanching the palm or sole of foot or
finger tips or toe tips—toe tips by applying pressure and then
assessing the time for return of color after the pressure is released.
4. Organ perfusion
a. Brain perfusion Brain perfusion can be assessed by features already
described in appearance, i.e. changes in level of consciousness,
pupil size, muscle tone and posturing.
b. Renal perfusion Urine output may not be useful in initial assessment
in a critically ill child, but is useful in monitoring and ongoing
assessment of the child and evaluation of renal perfusion. 1-2 ml/
kg/hour of urine output is normal
5. Blood pressure Shock can be present with normal, increased or
decreased blood pressure. In early compensated shock, BP is normal.
In late or decompensated shock there is hypotension.
Lower limit (5th percentile) of systolic blood pressure
Newborn 60 mm Hg
Upto 1 year 70 mm Hg
2-10 years 70 + (2 × age in years) mm Hg
Above 10 years 90 mm Hg
Based on the appearance, breathing and circulatory status, physiologic
status of a critically ill child is characterised as:
1. Stable
2. Respiratory distress characterised by IWB
3. Respiratory failure characterised by cyanosis, altered sensorium, poor
muscle tone and poor respiratory efforts.
4. Early shock—peripheral signs of shock with normal BP
5. Decompensated shock—peripheral signs with brain dysfunction and
hypotension
6. Cardiorespiratory failure—shock + respiratory failure
Conditions characterising a critically ill child requiring rapid cardio
pulmonary assessment
1. Tachypnoea Respiratory rate/minute
— > 60 in newborn
— > 50 in infants
— > 40 in 1-5 years
 Recognition and Initial Management of Critically Ill Child 193

2. Bradycardia or tachycardia
— Newborn < 80 and > 200 beats/minute (bpm)
— 1 month to 8 years < 80 and > 180 bpm
— > 8 years < 60 and > 160 bpm
3. IWB and decreased tidal volume
4. Cyanosis
5. Altered level of consciousness
6. Seizures
7. Fever with bleeding
8. Fever > 41°C in less than 3 months or fever in immunocompromised
child.
9. Trauma
10. Burns totaling > 10% body surface area
11. G1 bleeding
12. Poisoning

Initial Management of a Critically ill Child

When a child is assessed to be critically ill, initial management comprises
of taking care of airway, breathing and circulation. Recognition of acuity
of illness determines the urgency of intervention. Aggression in response
is driven by degree of physiologic compromise.
1. Airway is kept patent—if necessary by positioning, suctioning and
intubation.
2. Breathing In respiratory distress with increased WOB, only
supplemental O2 is given in a nonthreatening manner. This can be
done by nasal prongs, face mask or oxyhood.
If respiratory failure is present, positive pressure ventilation is done
with maximal supplementary oxygen.
3. Vascular access and volume expansion with isotonic fluids such as
Ringer lactate (RL) or normal saline (NS) if shock is present. If
peripheral venous access is not available an intraosseous access is
obtained just below the tibia.

Fig. 19.1: Bag mask ventilation

194 Selected Topics in Pediatrics for Practitioners

Fig. 19.2: Intraosseous access

4. Avoid oral feeds in a critically ill child.

5. If partial airway obstruction is suspected, allow the child to assume
position of comfort and avoid any painful procedure. Transport to a
centre where advanced airway management can be done including
foreign body removal.
6. If child presents with seizures, take care of airway and breathing and
control seizures with IV diazepam or lorazepam or midazolam. In
office practice, IM midazolam 0.15 mg/kg is safe, effective and fast.
7. In polytrauma or head trauma—open and maintain airway with
cervical spine stabilisation, carry out volume expansion with early
administration of blood and control obvious bleeding by external
compression. Early surgical/neurosurgical consultation is mandatory.
8. In acute severe asthma, nebulisation with salbutamol and if necessary
ipratropium. Administer oxygen early and monitor the child
periodically till improves.
9. Plan for transport to a centre where child can be managed further.
Common predisposing factors for a child becoming critically ill
1. Age: Younger the age, more the risk
2. Malnutrition/impaired immune status
3. Underlying anatomic/functional defect
4. Nature of illness
5. Bad child rearing/traditional practices
6. Type of medical care received
7. Parent’s knowledge/awareness

Preparedness to Manage Critically Ill Child

1. Oxygen source
2. Oxygen delivery system
 Recognition and Initial Management of Critically Ill Child 195

— Oxygen mask (infant, child size), non-rebreathing mask

— Nasal cannula, nasal prongs, oxygen hoods (Head boxes)
3. Suction apparatus/suction catheters 6G, 8G, 10G, 12G and 14G
4. IV cannula 20, 22, 24 size Scalp vein needles 21, 22, 23, 24 size
5. Intraosseous needles – 15 and 18 G
6. Fluids: Normal saline, lactated Ringer, 25% Dextrose, 10 Dextrose
7. IV sets
8. Self inflating bag (500 ml, 750 ml, 1500 ml), mask, reservoir bag
9. Drugs: Diazepam, Lorazepam, Hydrocortisone, Dexamethasone,
Dopamin, Inj Adrenaline 1:1000, Midazolam injections.
10. Nebuliser solution: Salbutamol, Ipratropium
11. Laryngoscope, blades (varying sizes)
12. Spine board
13. Drug dosage chart

Do’s and don’ts in management of critically ill child

Do’s
1. Be aware of age specific emergencies (e.g. bronchiolitis 3-9 months
of age).
2. Know about current epidemic in your area (e.g. dengue).
3. Keep emergency drugs ready and resuscitation equipment in good
condition and check every day if they are working.
4. List the telephone numbers of nearby hospitals and ambulance for
referral.
5. Inform parents about the problem and what is being done.

Don’ts
1. Don’t fail to monitor periodically
2. Don’t give only IV fluids without taking care of airway and breathing
3. Don’t give drugs by inappropriate route
4. Don’t panic.

BIBLIOGRAPHY
1. Fuhrman BP, Zimmerman JJ (Eds): Pediatric Critical Care (2nd edn), St.Louis,
Mosby 1998.
2. Pediatric Advanced Life Support Guidelines 1997 American Heart Association
and American Academy of Pediatrics.
3. Pediatric Emergency Medicine Course guidelines, Chennai 2001.
 20
Poisoning in Children
S Thangavelu

“The desire to take medicines is, perhaps, the great feature that distinguishes
man from other animals.”
Early identification and appropriate management is crucial—in saving
life and reducing morbidity. Toxic substances involved are predominantly
regional; because the availability is the major factor that decides the
substances involved. Household substances like kerosene are the culprits
in India when compared to medicines like calcium channel blocker and
tricyclic antidepressants in west. We must develop the strategies that are
relevant in our society and creat-resource base that provides answers for
the questions raised in the management of poisoning.

GENERAL MANAGEMENT
• Introduction and statistics
• When will you suspect poisoning
• Initial examination and resuscitation
• Reduction of toxin, absorption and elimination
• Lavage, charcoal and whole bowel irrigation
• Benign substances
• Antidotes
• Do’s and don’ts

MANAGEMENT OF SPECIFIC POISONS

• Kerosene
• Neem oil
• Rat killers
• Camphor
• Soap and detergents
• Naphthalene
• Button batteries
• Organophosphates
• Isoniazid
• Iron
 Poisoning in Children 197

• Dapsone
• Paracetamol
• Tricyclic antidepressants
The first part of this chapter comprised of general management of
poisoning and the second part about specific poisoning considered as
problems in our society. About 1-3% of the pediatric admissions are due
to poisoning, which may be on majority of occasions accidental, and in
a very small group due to intentional poisoning. They may present with
a chief complaint of toxic ingestion or present with unexplained
symptoms.
Two-thirds of the total poisoning exposures occurs in the pediatric
age group and among the children two-thirds are under five years of
age.
Incidence of poisoning ranges from 1.5-7 percent of the total pediatric
admissions. Majority of children with poisoning may not need hospita-
lization. Even among those hospitalized, only small number requires
emergency resuscitation and PICU admission. Mortality from different
hospitals ranges from 0.7-2.3 percent.

POISONING STATISTICS
(Institute of Child Health, Chennai-8)

Total Poisoning
Year hospital required Mortality % age
admission admission

1996 30582 607 20 3.29

1997 29506 649 13 2.00
1998 31246 646 09 1.39
1999 34343 767 18 2.34
2000 36282 710 12 1.69
2001 37747 772 05 0.64

POISONING—TYPE OF TOXINS
(Institute of Child Health, Chennai-8)

Type of poison 1996 1997 1998 1999 2000 2001

Drugs 120 119 103 113 153 123

Non-medicines 326 356 375 495 400 379
Envenomation and animal poisoning 141 152 143 149 139 226
(scorpion, snake, lizard in food,
insect bite)
Food poisoning 20 22 30 10 10 44

Total 607 649 651 767 710 772

198 Selected Topics in Pediatrics for Practitioners

Nature of toxin on substance consumed depends on region,

availability and age. Pesticide-exposure and snake bite are more common
in rural areas than in the urban. A pre-school-child with accidental
consumption of household substance is the most common scenario, but
rarely an adolescent may be brought with intentional poisoning with
multiple substances.
One should be knowledgeable about the common poisons consumed
in the region, local names, physical characteristics and the common
symptomatology.

When Will you Suspect Poisoning?

Usual scenario is a comatose child with vacuum in the history. Neither
the parents nor the relatives have any knowledge about what exactly
happened in the previous hours before some one saw the child in coma.
One should suspect unidentified trauma or poisoning in this situation.
Usual answer from a relative, when a physician asks about possible
toxin ingestion will be a big ‘NO’. We should try indirect questions:
• Does any one in the family take medicines?
• Can you check and account, the number of tablets kept at home?
• Problem oriented history
• Following information should be collected-description of toxin—
colour, odour, brand, and chemical name
• Magnitude—How much, number, volume
• Progression of symptoms
• Route, time of exposure
• Medical history—any underlying medical illness
• Initial care given
• Social back ground—any other person involved, predisposing reasons
for consumption.
These are four main goals in the management:
• Initial examination, resuscitation and basic supportive care
• Reduction of toxin absorption
• Toxin elimination
• Specific antidotes.
Among these, resuscitation and basic life support are the most
important and most commonly employed part of the management.
• Initial measures
• Cardiopulmonary assessment and resuscitation
• Assess the ABC’s and support the airway, ventilation oxygenation
profusion and as per PALS guidelines
• Certain modifications are to be done during resuscitation in a child
with poisoning.
• Intubation and ventilation.
 Poisoning in Children 199

Many toxins depress the CNS and leads to respiratory failure. One
should consider intubating poisoned patients earlier than they would
intubate for those without ingestion, because these children are at higher
risk.
Resuscitation drugs may need to be changed depending on the
poisonous substance. In organophosphate poisoning avoid using succinyl
choline for rapid sequence intubation because of the risk of prolonged
paralysis. Instead vecuronium or Rocuronium can be used.
• Avoid giving mouth-to-mouth respiration.
• Keep the patient in left lateral decubitus when they have spontaneous
respiration, both in emergency room and during transport to reduce
the risk of aspiration.
After resuscitation, look for any signs indicative of natural illness
and for features of poisoning – changes in mental status, smell of breath
(kerosene, camphor) pupillary changes, skin temperature, moisture of
mucus membranes, irregular pulse, breathlessness, blood in stools and
central cyanosis.
Status epilepticus, altered level of consciousness, requirement of
intubation and ventilation, hypotension, arrhythmia, DIVC are indicators
of serious poisoning.
Examination of a child with poisoning.
After the assessment of airway, breathing and circulation and
resuscitation, look for specific clinical signs
• Smell of breath Kerosene, camphor, naphthalene, alcohol,
• Miosis Organophosphate, opiate, barbiturates
• Mydriasis Dhatura, tricyclic antidepressants, cocaine
• Pallor Naphthalene
• Cyanosis Cardiorespiratory depression, methemoglobinemia
• Dry hot skin Dhatura, tricyclic antidepressants
• Convulsions Oral anti diabetic drugs, gamma benzene hexachloride,
organophosphates, INH, camphor, neem oil, theophylline, TCA,
antihistamine
• Bradycardia Beta blockers, calcium channel blockers, organo-
phosphates, tricyclic antidepressants, digitalis.
• Irregular pulse Tricyclic antidepressants, rodenticide
• Bleeding Oral anticoagulants, rodenticides, iron
• Following are characteristic clinical manifestation of specific poisons
200 Selected Topics in Pediatrics for Practitioners

Toxidromes

Symptoms and signs Poison

;
Large pupils, tachycardia, arrythmia, Dhatura, Tricyclic antidepressants
hallucinations and shallow breathing

Wet mouth, wet eyes, sweating, bradycardia, Organophosphates

diarrhea, small pupils, and convulsion
Small pupils, shallow breathing, coma Opiates
Coma, hypotension, bradycardia,
Bradypnea, hypothermia, bullous lesions Barbiturate, Diazepam

Reduction of Toxin Absorption and Elimination

Fresh air and skin decontamination is of tremendous value in cases of
toxic inhalation and skin exposure. Most of the toxins (particularly in
organophosphates) can be washed off with soap and water.
For GI decontamination, following methods are used.
Inducing emesis Though syrup of ipecac was widely used for a long
time in west (not freely available in India), now several studies have
shown that it is of no use.
In some places, salt (packet of salt mixed in a bucket of water) is used
to induce emesis. This may cause fatal hypernatremia and must never
be used.
Activated charcoal It is an inert, nontoxic and non-absorbable fine
black powder with vast surface area of fine network of pores. This
absorbs and traps the ingested poison so that it is passed out along with
charcoal in the faeces. More useful for poisons that are toxic in small
quantities like tricyclic antidepressants (TCA) and theophylline.
Maximum effect when it is given within one hour of ingestion. After one
hour of ingestion it may be still useful for sustained release preparations
and drugs that delay gastric emptying (e.g. TCA, opiates). Given after
mixing with water or fruit juice.

Recommended Dosage
Up to 1 year of age : 1 gram/kg
1-12 years : 25-50 gram
Dissolve each gram in 10-20 ml of water stir the activated charcoal
well with water until it looks like a thick soup. It can be also mixed with
fruit juice. Activated charcoal is given after the vomiting stops. In an
unconscious child it can be given through orogastric tube after ensuring
a stable airway or after intubation to avoid aspiration. More useful in
 Poisoning in Children 201

ingestion of TCA theophylline, paracetamol, isoniazid, beta blockers,

opiates and calcium channel blockers.
Not useful in iron poisoning.

Risks and contraindications Aspiration can occur and it is contraindicated

in unprotected airway or in the presence of ileus or intestinal obstruction.

Gastric lavage Maximum benefit is obtained when lavage is given within

one hour of ingestion but it is still considered after one hour of ingestion
if (1) A life-threatening amount has been consumed, or (2) Patient is
deeply unconscious because of poisoning or (3) For medicolegal purpose.
Less useful in removing intact tablets are larger fragments.
Before starting gastric lavage, ensure that powerful suction device is
immediately available. Elevate the foot end of the patient and place him
in left lateral position. It can be performed if there is a strong cough
reflex and in the absence, protect the airway with a cuffed ET tube. Use
aliquots of 15 ml/kg of normal saline (maximum 300 ml) and drain after
1 minute either by gravity or by applying suction. Preserve the first
sample for chemical analysis. Continue lavage until returning fluid is
clear. Administer charcoal after the lavage is completed before removing
the tube.

Controversy about gastric lavage Widely employed over 2 centuries and

was considered as one of the pillars of management of poisoning by
ingestion. There is no strong clinical evidence to support the view that
gastric lavage will benefit the patients who have ingested a poison.
Since the efficacy of removal by lavage decreases with time, it should
be considered only when life-threatening amounts of toxic agents was
ingested upto one hour previously. But in our environment, when other
techniques of decontamination such as activated charcoal are not easily
available, we cannot abandon lavage so lightly. At least we must be
aware about its complication and take enough precautions.
Risk and contraindication: The complications are hypoxia, esophageal
or gastrointestinal perforation. Lavage is contraindicated in corrosives
or hydrocarbon ingestion.
Antidotes are available only for minority of poisoning.

Whole bowel irrigation This is done by rapid administration of

polyethylene glycol electrolyte (PEGLEC) lavage solution through
nasogastric tube.
Useful in ingestion of iron and thallium where activated charcoal is
not useful. Also useful in sustained release preparations.
202 Selected Topics in Pediatrics for Practitioners

Rate of administration—15 ml/kg/h to a maximum of 500 ml/hr in

pre-school children and 1000 ml/hr in older children. Usually given till
the rectal effluent is clear.
Avoid in ileus, obstruction, perforation or significant GI bleeding.
Other methods of enhancement of excretion Methods like forced alkaline
diuresis are not used.
Just alkalinisation of urine is useful in ingestion salicylates, tricyclic
antidepressants and phenobarbitone. Dose: Sodium bicarbonate 2 ml/kg
start, followed by 1-2 ml/kg over 6 hours intravenously.
Dialysis Peritoneal dialysis is less effective. Hemodialysis is the treatment
of choice in salicylates, lithium, INH, methanol, ethylene glycol and
phenobarbitone (SLIME-P).

Antidotes
Antidotes are available only for minority of poisons.
Poison Antidote Dose Route Adverse
effects
warnings

Acetaminophen N-Acetyl- 140 mg/kg loading, then PO Nausea, vomiting

(Paracetamol) cysteine 70 mg/kg every 4 hrs,
17 doses
Benzo- Flumezanil 0.2 mg over 30 sec. IV Nausea, vomiting,
diazepines If inadequate response flushing, headache,
0.3 mg over 30 sec. If dizziness, seizures
inadequate response 0.5 mg
over 30 sec. No specific
dose for children

Beta blockers Glucagon 0.15 mg/kg IV Hyperglycemia,

bolus nausea vomiting
followed by
infusion of
0.05-0.1 mg/kg/hr
Cyclic Sodium IV
antidepressant Bicarbonate
Iron Deferoxamine Infusion of 15 IV Hypotension
mg/kg/hr (Minimised by
(Max—6 avoiding rapid
gram in 24 hr) infusion rates)

Isoniazid Pyridoxin Dose = Dose IV Uncommon

of isoniazid
25-50 mg/kg
IV repeat

Contd...
 Poisoning in Children 203

Contd...

Poison Antidote Dose Route Adverse

effects
warnings

Every 30
minutes till the convulsions
are controlled
Methanol Ethanol 750 mg/kg stat, IV/PO Nausea,
followed by 80-150 vomiting, sedation
mg/kg/hr
infusion of 5
or 10% ethanol
Methemoglobin- Methylene 2 mg/kg/show IV Nausea,
mia Blue infusion may vomiting
be repeated Headache,
every 60 min giddiness
(Max. dose 7 cyanosis,
mg/kg) haemolytic
anemia
Opiates Naloxone 0.01 mg/kg, if IV Acute
no effect withdrawal
0.1 mg/kg symptoms, if
repeat if addieted
needed
Organo- Pralidoxime 20-40 mg/kg IV Nausea,
phosphates (not used in in NS over headache,
carbamates) 30 min, can tachycardia,
be repeated muscle,
6-8th hrly if rigidity,
needed bronchospasm

Atropine 0.05 mg/kg IV/ET Tachycardia,

every 10 min, dry mouth,
as needed urinary
retention

KEROSENE INGESTION
Most common poisoning (about 50%) in Institute of Child Health,
Chennai and also in various hospitals all over India, because of
widespread availability and easy accessibility. It is common in toddlers.
Amount consumed can never be precisely determined.

Clinical Features
Develops symptoms in few minutes to hours. Early symptoms are—
Breath smelling of kerosene, distressing cough, fever, breathlessness,
drowsiness and restlessness because of hypoxia. This is followed by
204 Selected Topics in Pediatrics for Practitioners

chemical pneumonitis and bacterial pneumonitis. Pneumomediastinum,

pneumothorax and empyema are other complication.
Persistent altered sensorium and recurrent seizures are risk factors of
mortality according to one study. According to one study done in Sri
Lanka, out of 520 children with kerosene ingestion, 3 children died and
none of them developed neurological symptoms despite 75 percent of
them developed pneumonia. This is probably related to the composition
of kerosene.

Mechanism
Displacement of alveolar gas by vaporized kerosene leading on to
hypoxia, destruction of surfactant leading to atelectasis and emphysema,
local damage causing destruction of septa and alveolar wall are the
mechanisms by which respiratory tract is damaged.

Management
X-ray abnormalities may not be apparent initially, but most will show
changes within 12 hours. They may not correlate well with clinical
features.
Initial management in emergency room is giving oxygen through
mask or hood. Gastric lavage or inducing emesis is contraindicated. In
initial stages, respiratory distress may appear because of chemical
pneumonitis. As there is no definite way to differentiate chemical
pneumonitis from bacterial pneumonitis, it is better to start antibiotics.
CNS depression causing shallow breathing or apnea, severe respiratory
distress with de-saturation or development of pulmonary edema are
indications for ventilatory support. High-risk of barotrauma should
always be kept in mind during ventilation.
Generally prognosis is very good once oxygenation and ventilation
are taken care of:
Case history: 1½-year-old girl accidentally consumed kerosene kept in
mineral water bottle at her house at 5:30 PM. Mother noticed after few
minutes, when the girl started developing severe cough and vomiting.
She was rushed to a nearby clinic. After giving an injection she was
referred to the hospital.
Brought to emergency room at 7:30 PM. She was comatose, with
irregular respiration and absent Doll’s eye movements. Pupil was
constricted and she was in a state of hypotension and shock. Extensive
crepitations were heard on auscultation. Managed with ventilatory
support, fluid resuscitation and inotropes. This child died after 5 hours
of stay in the hospital.
 Poisoning in Children 205

NEEM OIL INGESTION

It is one of the innocent acts leading on to a serious fatal complication.
It is a traditional practice in villages and in some urban houses to
administer neem oil. It is done with a wrong belief that it is a remedy
for worm infestation and respiratory problem.
It is not very clear whether neem oil per se is responsible for the toxic
symptoms or it is due to any contaminating chemicals.

Clinical Features
Usually symptoms develop within 10-60 minutes. Vomiting followed by
convulsions which are often refractory requiring multiple drugs to
control. Some develop respiratory failure and may require ventilatory
support. Serious poisoning can lead on to death or neurological sequelae.

Management
• Management is supportive
• Control of seizures
• Careful monitoring and management of ventilation with ventilatory
support.
Case history: 70 days old girl. JR was administered neem oil about a
spoonful at 7.00 AM with the belief that it will cure her cold and cough.
After 15 minutes she developed vomiting and seizures. Brought to
emergency room with seizures. She required two doses of lorazepam,
phenytoin and phenobarbitone. Intubated and and admitted in PICU.
Convulsions lasted for 14 hours and got controlled with midazolam
infusion 8 mcg/kg/hour. She was on ventilatory support and was weaned
after 7 days. Got discharged well later.

RAT KILLER POISON

Rodenticides are commonly available in the house, and easily accessible
for children. Following chemicals are used us rodenticide:
• Aluminium phosphide
• Zinc phosphide
• Warfarin like compounds
• Arsenic salts
• Thallium and strychnine (? available in our region).

Aluminium Phosphide and Zinc Phosphide

These are used as rodenticide and grain preservatives. When swallowed,
releases phosphine gas in the gut and causes toxic effects.
206 Selected Topics in Pediatrics for Practitioners

They cause ARDS, hypoxemia, myocarditis, cardiac arrythmia and

conduction disturbance, pulmonary edema, acute renal failure, hepatitis
and disseminated intravascular coagulation. Sometimes raised serum
magnesium levels are observed.

Treatment
Gastric lavage is useful. Treatment is mainly supportive. Diuretics,
inotropes and ventilatory support. Hydrocortisone for myocarditis.
Warfarin like chemicals After ingestion bleeding from multiple sites
develops after 12-48 hours. Monitor by doing prothrombin time. Managed
with intravenous vitamin K, fresh frozen plasma and blood transfusion
if there is significant blood loss.
Case history: Four months old girl patient was administered rat killer by
mother in a mass family suicide. Neighbour saw the child after about
3 hours in an unresponsive state and throwing convulsions and brought
to the hospital in a comatose state (GCS 4). Constricted pupil, hypotonia
and jerky respiration were observed. Intubated in emergency room and
was ventilated.
About 12 hours after ingestion, child developed bleeding in the
nasogastric aspirate and shock. Managed with FFP, packed RBCs and
dopamine. Next day child developed pneumonia and worsening of
shock state requiring epinephrine infusion. Investigations showed
hypoglycemia, acidosis, raised hepatic enzymes and normal bilurubin.
Child continued to have seizures, shock and respiratory failure and died
on 4th day after ingestion.

INGESTION OF SOAP AND DETERGENTS

Soaps are natural products made from animal or vegetable fat or oils.
Detergents are synthetic chemicals used as cleaning agents.

Three Groups of Detergents

Non-ionic and anionic detergents are harmless except the automatic
dishwasher detergents. Cationic detergents are more harmful and may
cause death.
Anionic detergents used for washing dishes, clothes or hair or for
general household cleaning.
Nonionic detergents—used in low lather laundry products.
Cationic detergent—used as antiseptics and disinfectants in the home,
food industries and hospitals which are benzalkonium, cetrimide, cetyl
pyridinium, dequalinium.
 Poisoning in Children 207

Clinical Features
Soap, nonionic and anionic detergents Soreness of mouth, swelling of lips
and mouth, vomiting and diarrhea.
Cationic detergents Burns in the mouth and throat, vomiting and diarrhea,
muscle weakness, altered level of consciousness, convulsion,
hypoventilation, hypotension, pulmonary edema and serious burns in
the eye.

Management
Initial measures—wash the eyes and skin with water, give a cup of
water to drink. Supportive management of airway and breathing, shock
correction and treatment for pulmonary edema.

CAMPHOR POISONING
Traditional practice of application of camphor over chest and back and
oral administration for the treatment of respiratory infection is responsible
for camphor poisoning. Vomiting, convulsions, restlessness and apnea
may develop within an hour. Generally improvement occurs in a day
or two after the control of seizures with anticonvulsants. In the initial
management, charcoal may be useful.
Case history: Nine-months old boy was administered camphor with
external application over back for cough and cold at 9:00 AM. After ½
an hour, he developed two episodes of convulsion, brought to emergency
room with seizures, got controlled with one dose of lorazepam. There
was no recurrence and fully became alert after 24 hours.

NAPHTHALENE
It is a common hydrocarbon easily available for the children at home.
Toxic metabolite is alphanaphthol, which causes hemolysis resulting in
hepatic and renal damage. Acute hemolytic anemia, nausea, vomiting
and abdominal pain due to gastric irritation, renal colic, hemoglobinuria,
jaundice, nephritis, methemoglobinemia and convulsion are seen.

Treatment
Lavage and activated charcoal are useful. Avoid giving milk that may
promote absorption. Alkanizing urine with bicarbonate, hydrocortisone
to limit hemolysis, blood transfusion, intravenous methylene blue if
there is methemoglobinemia, management of hepatic failure and renal
failure are useful.
208 Selected Topics in Pediatrics for Practitioners

In one study out of 3 children admitted for naphthalene ingestion,

only one child, 1½ year old developed jaundice, evidence of hemolysis,
altered sensorium and died within 12 hours. Even one moth ball ingestion
has proved fatal in a child.

INGESTION OF BUTTON BATTERIES

Ingestion of button batteries causes problems by (1) Mechanical
obstruction (2) Corrosive damage, (3) Electrical discharge, (4) Mercury
poisoning from leaking batteries. Problems are less with old spent battery
than from new ones.

Management
Check by X-ray
Battery in the nose should be removed as soon as possible. It causes
corrosive burns, bleeding and septal perforation.
Battery in oesophagus should be removed immediately using
endoscopy, foley catheter or a magnet.
Battery in the stomach should be removed, if they are leaking, causing
symptoms (pain diarrhea, bleeding) or have been present for several
days.
Need not be removed if battery is intact and not causing symptoms,
since many batteris pass out uneventfully. Take repeat X-ray to see the
position and to see if it is disintegrating. But these can be retrieved
without anaesthesia using orogastric magnets and fluoroscopy.
Battery in small or large bowel—usually passes spontaneously. Should
be removed if they open or cause symptoms. If removal is needed,
consider whole bowel irrigation before surgery.
If battery is disintegrating, check mercury levels.

ORGANOPHOSPHORUS POISONING
Common poisoning in adults and adolescents particularly in rural areas,
Children are given this poison when the family attempts a mass suicide.
These compounds cause toxic symptoms by binding acetylcholinesterase
irreversibly. They are rapidly absorbed through intact skin, inhalation
or ingestion.

Compounds
Parathion, (Folderol, Ekatox, Killphos) Malathion (Kill bug,
bugsolime 20). Diazimon (Diazion, TIK-20).
 Poisoning in Children 209

Clinical Features
Three types of toxic effects observed.

CNS Stimulation
Restlessness, seizures, coma and cardiorespiratory depression.

Nicotine Like Effects

Fatigue, muscle cramps, neuromuscular block and paralysis including
muscles of respiration.

Muscarine Like Effects

Excessive secretions-salivation, lacrimation, involuntary urination and
defecation, vomiting, bronchospasm, bronchorrhea,, bradycardia and
heart block.
Cardiorespiratory failure is the cause for fatality.

Diagnosis
Mainly clinical by history or by typical clinical features. Estimation of
plasma and RBC cholinesterase which may show a fall.

Complication
Pulmonary edema, ARDS, aspiration pneumonia, respiratory failure.
Preferably avoid phenothiazines, morphine, antihistamine and
aminophylline.

Management
Initial measures—remove the soiled cloth, washes skin with soap and
water. Gastric lavage and administration of activated charcoal.
Intravenous atropine 0.05 mg/kg IV every 10 minutes until atropine
toxicity occurs (Drying of secretions to be considered rather than dilated
pupil) then reduce the frequency every ½ an hour, one hour, two hours
and four hours, then stop after 24, 48 hours.
Pralidoxime or 2-PAM—Mainly counteracts the effects of nicotine
like effects, can also be given when only muscarinic effects alone are
present. It has a synergistic effect with atropine. Dose 20-40 mg/kg in
normal saline over 30 minutes. Can be repeated every 6-8 hourly till the
nicotinic effects subside. P2AM is not indicated in carbamate poisoning.
Ventilator support when GCS is very low, or breathing is shallow.
210 Selected Topics in Pediatrics for Practitioners

INH POISONING
This is one of the serious poisons that can cause death. Liquid preparation
is more likely to be consumed than tablets.

Clinical Features
Toxic symptoms can develop within 30 minutes to 3 hours which are
nausea, vomiting, slurred speech, convulsions, altered level of consciou-
sness, shock and shallow breathing. Complications of severe poisoning
includes lactic acidosis, ketoacidosis, hyperglycemia, renal failure.

Management
Monitor vital signs, glucose, electrolytes, renal function and liver function.
Supportive care—management of shock with fluid resuscitation and
inotropes. Correct the dyselectrolytemia and acidosis. Control of seizures.
Ventilatory support.
Antidote Intravenous pyridoxin 25-50 mg/kg over 5 minutes. Can be
repeated every 30 minutes until the convulsions are controlled or the
child is awake.
Case history 1½ years old boy consumed about 50 ml of INH syrup,
about 1.5 grams at 10:00 AM. Then developed vomiting and convulsions
at 12:00 noon. Brought to emergency room at 2:30 PM in a state of shock,
status epilepticus, jerky respiration and low oxygen saturation. Intubated
and ventilated. As the patient did not respond to fluid boluses, dopamine
started. Shock improved and spontaneous respiration established after
24 hours. Next 24 hours he was drowsy, head-lag was present. After 48
hours child became alert and started taking feed.

IRON POISONING
Iron ingestion is always considered as potentially dangerous, because
toxic dose is not absolute. However significant toxicity is uncommon in
amounts, less than 60mg/kg. Lethal dose is between 200-250 mg/kg.

Clinical Feature
It acts in the body as a metabolic poison. Primarily it affects the gastro-
intestinal tract, liver, cardiovascular system and brain. Five stages are
observed, following iron poisoning.
I. Gastrointestinal stage (30 minutes-2 hours) Vomiting, diarrhea,
abdominal pain and gastrointestinal bleeding.
II. Stage of relative stability (2-6 hr) This is a poorly defined stage in
which child appears better, when gastrointestinal symptoms
ameliorate and overt shock not yet developed.
 Poisoning in Children 211

III. Circulatory Failure (6-12 hr) This stage is characterized by shock,

which is multifactorial in origin. Profound shock, depressed
sensorium, acidosis and coagulopathy develop at this stage and
are responsible for the fatality.
IV. Stage of hepatotoxicity (2-4 days) Characterized by elevation of hepatic
enzymes and bilirubin with prolonged prothrombine time.
V. Stage of gastrointestinal scarring (2-4 weeks) Scarring observed in the
pyloric region.

Diagnosis
History, abdominal X-ray for presence of radiopaque material.
(iron tablets).
Biochemistry—hypoglycemia, raised hepatic enzymes and bilirubin,
prolonged prothrombin time and metabolic acidosis.
Free serum iron estimation at 6 hours after ingestion.
Free serum iron = Total serum iron – Total iron binding capacity. If
serum free iron is 50 mg/dl or more or total iron above 350 mg indicates
severe toxicity.

Management
Admit in intensive care unit, gastric lavage should be done and charcoal
administration is not beneficial. Whole bowel irrigation is considered to
be the technique of choice. GI decontamination is not needed when
X-ray is negative. Gastrotomy may be needed in massive overdosage.
Negative X-ray in an asymptomatic patient excludes significant
ingestion. But X-ray may be negative in a symptomatic patient due to
following reasons.
Iron well dissolved or absorbed liquid iron preparation or small
amount of iron in a multivitamin preparation.

Investigation includes: CBC, electrolytes, liver function test, blood group,

renal function test coagulation screening and serum iron.
Fluid resuscitation and correction of acidosis is the primary therapy
for iron intoxication. Large amount of bicarbonate may be needed. Blood
transfusion or fresh frozen plasma wherever indicated.
Chelation is indicated in a symptomatic patient. Deferoxamine is
given in the dose of 15 mg/kg/hour intravenously to a maximum
cumulative doses of 6 G. Following chelation, urine colour change to
rose, pink colour because of the excretion of iron deferoxamine complex.
Stop chelation when the urine colour becomes normal, or when the
symptoms subside.
212 Selected Topics in Pediatrics for Practitioners

Case history 2½ year old boy R consumed about 10 tablets of iron

prescribed for his mother which was kept down in the floor probably
around 5.30 PM. At 7.00 PM he became drowsy, developed crying spells
and passed black stools. He has consumed about 100 mg/kg. Brought
to emergency room in a state of shock and altered sensorium. X-ray
showed radiopaque shadows indicating the presence of iron. Shock
improved with two RL boluses. Gastric lavage was done. Deferoxamine
was started and the urine colour changed to reddish colour. On third
day he developed abdominal pain and jaundice. Hepatic enzymes were
raised 492 IU and 300 IU. Serum iron could be done only on II day
(ideally at 6 hours), which was 170 mg. He was reviewed in the
gastroenterology department after 6 weeks. Endoscopy was done and
no stricture was seen.

DAPSONE POISONING
Dapsone causes oxidation of iron from ferrous to ferric state resulting
in the formation of methemoglobin, end result is decreased oxygen
binding and impaired oxygen delivery.

Clinical Features
Irritability, restlessness, slate gray central cyanosis without any cardio-
respiratory illness, cyanosis not improving with oxygen supplement.
Laboratory diagnosis Bedside diagnosis—comparing the colour of the
patient’s blood (by placing a drop of blood in the filter paper) with
control. Patient’s blood will show a chocolate brown colour but the
control blood drop is bright red. Even a drop of blood from a cyanosed
patient due to cardiac or respiratory cause will turn bright red on
exposure to air (spectrophotometry and methemoglobin assay). Levels
> 10 percent, patient will be symptomatic. Severe symptoms when levels
are higher.

Other investigations are spectrophotometry and methemaglobin assay.

Treatment
Gastric lavage, activated charcoal oxygen administration and intravenous
methylene blue 2 mg/kg diluted in normal saline slowly over 5 minutes
(dilution is done to make the concentration to 1 mg/ml. Available as 1%
methylene blue, specially prepared solution for intravenous use) can be
repeated every 60 minutes to a maximum cumulative dose of 7 mg/kg.
Intravenous ascorbic acid is also useful.
Exchange transfusion if levels are very high or if symptoms persist.
 Poisoning in Children 213

Case history Three years old boy K was brought to the hospital casualty
in the evening in altered consciousness. He was irritable, crying, and
mildly tachypneic and was cyanosed. Mother has given him fish in the
noon; during eating she removed a fish bone from the mouth. For the
next few hours, she was busy doing her farm work and hence was not
sure about her son’s whereabouts. Later in the evening, she found him
lying down unconscious outside her house in the street. She denied any
history of injury or drug ingestion.
Because of central cyanosis, mild tachypnea and fish bone removal,
foreign body obstruction of the airway was considered as the first
possibility. Bronchoscopy was done and no foreign body was detected.
Second possibility considered was Methemoglobinemia, because of
absence of respiratory distress or other cardiorespiratory signs and
chocolate brown colour of the blood. Normal chest X-ray, ECG, ECHO
and raised Methemoglobin level of 45 percent confirmed the diagnosis.
He was successfully treated with IV methylene blue and vitamin C. This
could be due to an unproven dapsone ingestion.

PARACETAMOL POISONING
Paracetamol poisoning causes serious liver damage and renal tubular
necrosis. When more than 150 mg/kg in children and above 12 gm in
adult is consumed.

Mechanism
A metabolite of paracetamol binds glutathione in the liver and causes
hepatic necrosis.

Clinical Features
• I stage (½-24 hr) nausea, vomiting, pallor, diaphoresis
• II stage (24-48 hr) right upper quadrant abdominal pain and
tenderness and oliguria. Elevated hepatic enzymes, prothrombin time
and bilirubin
• III stage (72-96 hr) hepatic failure-jaundice, coagulopathy
encephalopathy, renal failure.
• IV stage (4 days-2 weeks) resolution or complete liver failure.
• Lab. estimation—plasma drug level should be measured at 4 hours
or later and should be plotted on the nomogram to decide about the
treatment.
214 Selected Topics in Pediatrics for Practitioners

Management
Initial Measures
Gastric lavage, activated charcoal and cathartics.
Antidote is N.acetyl cysteine given intravenously. 150 mg/kg in 5%
dextrose over 15 minutes. Then 50 mg/kg over 4 hr, than 100 mg/kg
over 16 hr.
Oral or orally 140 mg/kg followed by 70 mg/kg every 4 hrs × 17 doses.
Dilute NAC with fruit juice as 5% solution. If vomiting occur within one
hour, repeat with an antiemetic.
Intravenous and oral preparations are equal in efficacy, but IV route
can be given within a shorter period.

TRICYCLIC ANTIDEPRESSANT (TCA) POISONING

TCA produces severe neurological and cardiovascular toxicity. Toxicity
is seen at the dose of 10-30 mg/kg.

Drugs
Amineptine, amitriptyline, amoxapine, clomipramine, dothiepin,
doxepin, imipramine nortriptyline, trimipramine.

Clinical Features
Depression of consciousness, seizures, hypoventilation and respiratory
arrest. Quinidine like effect over heart, causing tachycardia, dysrythmia,
myocardial depression, shock, ECG changes—QRS widening, QT
prolongation, ST depression, T wave inversion, Right bundle branch
block and complete heart block.
Dilated pupil, dry mucus membranes and other features of anti-
cholinergic syndrome.

Management
Usually requires ICU care.
Initial measures support the airway, breathing circulation first—then
gastric lavage, activated charcoal.
Asymptomatic patients may be monitored for 12-24 hr.
Alkalinisation using bicarbonate, maintain pH between 7.45-7.55 to
prevent and treat dysrythmia. Lidocaine is used if dysrhythmia already
exists or develops despite alkalinisation. Phenytoin is needed when
bicarbonate and lidocaine fails to correct dysrhythmia.
 Poisoning in Children 215

In shock management with fluid resuscitation, use 10 ml/kg instead

of standard 20 ml/kg because of myocardial depressant effect of TCA.
Norepinephrine may be preferred over dopamine because of depletion
of catecholamines. Though epinephrine is also equally effective, less
preferred because of arrythmogenic property.
Physostigmine is an exceptionally dangerous agent and should not
be used.
“A search-light cannot be used effectively without a fairly thorough
knowledge of the territory and target (Toxin) to be searched.”

POISON INFORMATION CENTERS

Intensive medical care unit, Govt. General Hospital, Madras Medical
College, Chennai
Tel: -44-25363208;
All India Institute of Medical Sciences, New Delhi
Tel: -11-26850691, 26159391, 26593677

BIBLIOGRAPHY
1. Durairaj A. Clinical management of poisoning and Medical Toxicology.
I edition, 1993.
2. For further reading Suchitra Ranjit, Essentials of pediatric critical care, Paras
Publishing 2002.
3. Henry J, Wiseman H. Management of Poisoning. A Handbook for Health Care
Workers World Health Organization 1997.
4. PALS provider Manual published by American Academy of Pediatrics and
American Heart Association, 2002.
5. Richard E, Behrman, Robert M, Kliegman, Hal B Jenson. Nelson Textbook of
Pediatrics, WB Saunders Co (16th edn), 2000.
6. Utpal Kant Singh, FC Layland, Sanjay Suman, Rajhiti Prasad, Poisoning in
children, Jaypee II edition 2001.
 21
Rational Drug Therapy
in Pediatric Practice
A Parthasarathy

INTRODUCTION
Once a practitioner remarked thus to his fellow pediatrician: “ What is
irrational to you may be rational to me”. In these days of ‘poly pharmacy’
with eagerness and enthusiasm to prescribe newer drugs and vaccines
introduced in the market one has to ask the following questions before
issuing a prescription:
1. Is a drug essential for this illness?
2. If so, have I chosen the right drug?
3. Have I prescribed the drug at the right dosage, frequency and
duration?
4. Am I wellversed with the pharmacokinectics and adverse effects
of the drug which I am prescribing?
5. Do I know how to manage if an adverse effect manifests?
6. Do I have facilities for cardiorespiratory resuscitation in case of
anaphylaxis?
7. Am I using a banned drug? Irrational combination?
8. Am I to inform any adverse event to the drug regulatory authority?
9. Am I prescribing an ayurvedic or homeopathic drug?
10. Have I gone through the literature/scientific information provided
by the manufacturer before prescribing the drug?

Guidelines on the Use of Drugs in Children

While administering drugs to children, particularly neonates (first 30
days of life), special care is always needed because they differ from
adults in their response to drugs. Doses should invariably be calculated
on the basis of weight. In the neonatal period, the risk of toxicity is
higher due to inefficient renal enzymes, heightened sensitivity and
inadequate detoxifying mechanism.
If possible, painful intramuscular injections should be avoided. It is
always a good practice to state the age of child patient while writing
prescriptions. Even though liquid preparations are more commonly used
they contain sucrose, which can lead to dental decay.
 Rational Drug Therapy in Pediatric Practice 217

Dosage
Children’s doses are prescribed pertaining to the following age ranges:
Neonate (first month), infant (up to 1 year), 1-5 years and 6-12 years.
Where a single dose is given, it applies to the middle of the age range.
Hence adjustment would need to be made for lower and upper limits
of the stated range.

Dose Calculation
The dosage for children can be calculated from adult doses by using
either age, or body-weight or body surface area or by a combination of
these factors. Even though body-surface area provides the most reliable
method of determining dosages, in practice it is exceedingly difficult.
Body-weight can be easily used to calculate doses and are generally
expressed in mg/kg. Because of their higher metabolic rate, children
generally require higher dose per kilogram than adults. This method
can pose problems while calculating dose for obese children since they
are liable to be given higher than required dose. Under such circum-
stances, it is better to calculate dose based on ideal body weight of the
child in that particular age.

Body Surface Area (BSA)

It is technically better and more accurate since many physical pheno-
mena are more closely related to body surface area. The average body
surface area of a 70 kg adult is about 1.7 to 1.8 square meter. Thus to
calculate the dose for a child the following formula is used:
Surface area of child (m2) × adult dose
______________________________________
Approximate dose for child =
1.8

The Percentage Method as given below can be conveniently used to

calculate dose for children when there is wide margin between therapeutic
and toxic dose:
Age Ideal body weight Height Body-surface Percentage of adult dose

Newborn 3.4 kg 50 cm 0.23 m 12.5%

1 month 4.2 kg 55 cm 0.26 m 14.5%
3 month 5.6 kg 59 cm 0.32 m 18%
6 month 7.7 kg 67 cm 0.40 m 22%
1 year 10 kg 76 cm 0.47 m 25%
3 years 14 kg 94 cm 0.62 m 33%
5 years 18 kg 108 cm 0.73 m 45%
7 years 23 kg 120 cm 0.88 m 50%
12 years 37 kg 148 cm 1.25 m 75%
218 Selected Topics in Pediatrics for Practitioners

Dose Frequency
Doses of antibiotics are usually prescribed at intervals of 6, 8, or 12
hours in children. Some flexibility may be allowed so that they are not
woken up at night. In the case of new drugs, the recommended doses
must not be exceeded.

IRRATIONAL COMBINATIONS
Dubious fixed-dose combinations (FDCs) are being marketed in India
but not approved in any developed country. Most of these combinations
are not approved by the Drugs Controller General, India and hence
illegal.
• Alprazolam + Sertraline
• Alprazolam + Imipramine
• Alprazolam + Fluoexetine
• Alprazolam + Melatonin
• Imipramine + Diazepam
• Risperidone + Trihexypenidyl
• Norfloxacin + Tinidazole
• Norfloxacin + Tinidazole + Dicyclomine
• Norfloxacin + Tinidazole + Loperamide
• Norfloxacin + Metronidazole
• Norfloxacin + Ornidazole
• Ciprofloxacin + Tinidazole
• Ciprofloxacin + Metronidazole
• Ofloxacin + Tinidazole
• Ofloxacin + Metronidazole
• Ofloxacin + Ornidazole
• Fluconazole + Tinidazole
• Doxycycline + Tinidazole
• Tetracycline + Metronidazole
• Tramadol + Paracetamol
• Mefenamic Acid + Drotaverine
• Mefenamic Acid + Tizanidine
• Nimesulide + Drotaverine
• Nimesulide + Paracetamol
• Nimesulide + Diclofenac
• Nimesulide + Dicyclomine
• Nimesulide + Chlorzoxazone
• Nimesulide + Methocarbamol
• Nimesulide + Camylofin
• Nimesulide + Serratiopeptidase
• Nimesulide + Tizanidine
 Rational Drug Therapy in Pediatric Practice 219

• Nimesulide + Paracetamol + Chlorzoxazone

• Nimesulide + Tizanidine + Paracetamol
• Nimesulide + Cetirizine + Psuedoephedrine
• Tizanidine + Paracetamol
• Rofecoxib + Tizanidine
• Ibuprofen + Tizanidine
• Diclofenac + Tizanidine
• Diclofenac + Famotidine
• Diclofenac + Paracetamol + Tizanidine
• Diclofenac + Serratiopeptidase
• Diclofence + Paracetamol + Serratiopeptidase
• Diclofenac + Fenpiverinium + Pitofenone
• Ibuprofen + Paracetamol + Magnesium trisilicate
• Ranitidine + Dicyclomine
• Sucralfate + Oxethazine
• Cisapride + Omeprazole
• Mosapride + Methylpolysiloxane
• Magaldrate + Simethicone + Oxethazine + Dicyclomine
• Diazepam + Dried Aluminium Hydroxide Gel + Aluminium Glycinate
+ Oxyphenonium
• Diazepam + Dried Alum
• Hydrox.Gel + Magnesium Trislicate + Dimethylpolysiloxane
• Diapezam + Magaldrate + Oxyphenonium
• Diazepam + Propantheline + Dihydroxy Alum
• Pipenzolate + Phenobarbitone
• Amoxycillin + Cloxacillin + Lactobacillus + Serratiopeptidase
• Amoxycillin + Serratiopeptidase
• Amoxycillin + Probencid + Tinidazole
• Cefuroxime + Serratiopeptidase
• Roxithromycin + Ambroxol
• Ciprpofloxacin + Ambroxol
• Cefoperazone + Sulbactum
• Ramipril + Losartan
• Enalapril + Losartan
• Amlodipine + Lisinopril
• Amlodipine + Enalapril
• Amlodipine + Ramipril
• Amlodipine + Losartan
• Amlodipine + Atenolol
• Atenolol + Alprazolam
• Propranolol + Alprazolam
• Propranolol + Diazepam
• Cinnarizine + Domperidone
220 Selected Topics in Pediatrics for Practitioners

• Domperidone + Ranitidine
• Domperidone + Omeprazole
• Domperidone + Famotidine
• Domperidone + Pantoprazole
• Domperidone + Lansoprazole
• Mebendazole + Pyrantel
• Mebendazole + Levamisole
• Simvastatin + Nicotinic Acid
• Loratadine + Ambroxol
• Cetirizine + Ambroxol
• Cetirizine + Dextromethorphan + Phenylpropanolamine
• Ceitrizine + Paracetamol + Phenyl Propanolamine
• Clopidrogel + Aspirin
• Glimepirride + Pioglitazone
• Montelukast + Bambuterol
• Tranexamic Acid + Etamsylate
• Tranexamic Acid + Mefenamic Acid

Rational Drug/Antimicrobial Therapy—Examples

Given below are some examples of rational drug/antimicrobial therapy
in common pediatric illnesses.
1. Acute Respiratory Infection.
• Acute Pharyngitis
• Otitis Media
• Community acquired pneumonia (CAP)
• Hospital acquired pneumonia (HAP)
2. Acute Dysentery and Invasive Diarrhea
3. Urinary Tract Infection.
• Let us first see, the antibacterial sensitivity to common pathogens
responsible for most URTI’s and LRTI’s in OP management.

Antibiotics in Outpatient Management of CAP—Spectrum of Action

Antibiotic S pneum H infl Staph Myoplasma Chlamydia Legionella

Cotrimoxazole + + - - - + /-
Penicillin + - - - - -
Ampi/Amox + + - - - -
Amoxiclav + + + - - -
I Cephalo + + /- +
II Cephalo + + + /-
III Cephalo + + + /-
Macrolides + /- - - + + +

Duration of Therapy 7-10 days. Azithromycin 3-5 days.

 Rational Drug Therapy in Pediatric Practice 221

Antibiotics in Hospitalised Patient Management of CAP

Age Pathogens Antibiotics/combinations

0-3 months GBS, Listeria CP + Genta

Gram Negative Ampi + Genta
Staph Cefotaxime/ampi
Chlamydia Erythromycin

Infants S. pneum; Hib Cefotaxime

Staph, GAS Clox + Genta
Kleb’s Cefazolin + Amikacin
Chlamydia Erythro/Azithro/Clarithro

Children > 5 yrs S. pneum, Hib, Staph Co amoxiclav/Cefuroxime

Mycoplasma Erythro/Azithro
Chlamydia } Clarithro

Antibiotics in Other Situations

Situations Presumptive pathogen Suggested Antibiotics

HAP Staph aureus Cloxacillin, Vancomycin

Cefotaxime/Ceftriaxone
Gram Neg. E Coli, Klebsiella Aminoglycosides + Ceftazidime

Pseudomonas Piperacillin + Metronidazole

Clindamycin, Cefoxitin
Opportunistic infection Pneumocystis Cotrimoxazole
Fungi Fluconazole
Myc. tub 2HRZE/4 HR (7HR)

Viral HSV Acyclovir

Aspiration pneum Anaerobes Coamoxi – Clav, Metro + Ampi
Oral Commensals Clinda, Piperacillin

Duration of Therapy (IV + PO) 14 days—21 days

In Presence of Complications 4-6 weeks

Antimicrobials Dosage Route and Frequency of Administration

Cryst. Pencicillin 2,00,000 u/kg/dQ6H

Ampicillin 150 mg/kg/dQ6H
Amoxicillin 30-90 mg/kg/dQ8H
Amoxiclav 30 mg/kg/dQ12H
Cloxacillin 150 mg/kg/dQ6H
Cefazolin 100 mg/kg/dQ6H
Cefotaxime 150 mg/kg/dQ8H
Ceftrioxone 150 mg/kg/dQ12H
Ceftazidime 100 mg/kg/dQ12H
Cefuroxime 150 mg/kg/dQ8H
Gentamycin 5-7 mg/kg/dQ8H
(4mg/kg/d single dose in small infants)

Contd...
222 Selected Topics in Pediatrics for Practitioners

Contd...

Amikacin 10-15 mg/kg/dQ12H

Erythomycin 50 mg/kg/dQ6H
Azithromycin 10 mg/kg/D1, 5mg/kg/D2 – D5 Q24H
Clarithromycin 15 mg/kg/dQ12H.P.O
Cotrimoxazole As TMP 5-8 mg/kg/ d} Q12H
Sulpha 40 mg/kg/d}
Vancomycin 40 mg/kg/d IV Q6H (over 60 minutes
infusion)
Clindamycin 20 mg/kg/dQ6H I.V
Metronidazole 15-20 mg/kg/dQ8H PO/ IV
Fluconazole 3-6 mg/kg/dQ24H PO/ IV
Acyclovir 30 mg/kg/dQ8H

The following tables describe the specific pathogen susceptibility

and choice of antimicrobials, their dose and duration in infections
encountered commonly in pediatric practice:

Specific Pathogens Amenable to Antimicrobial Prophylaxis

Pathogen Disease to be prevented Antimicrobial Efficacy

agent

Bacteria
Bordetella pertussis Secondary cases of pertussis Erythromycin Established
in household contacts
Chlamydia trachomatis Urogenital infections in Tetracycline* Proposed
exposed persons erythromycin
Corynebacterium Diptheria in unimmunised Penicillin, Proposed
Diphtheriae contacts Erythromycin
Haemophilus influenzae Secondary cases of systemic Rifampin Established for
type b infection in close contacts< 4 y household
Mycobacterium Overt pulmonary or Isoniazid Established
tuberculosis metastatic infection
Neisseria gonorrhoea Penicillin—resistance gono- Ceftriaxone Established
ccoccal infection in exposed
persons
Streptococcus Fulminant pneumococcal Penicillin Established for
pneumoniae infection in those with penicillin V in
asplenia children with
sickle-cell anemia
Group A streptococcus Recurrent rheumatic fever Penicillin, Established
sulfadiazine
Group B streptococcus Neonatal infection Ampicillin Established
(intrapartum)
Vibro cholerae Cholera in close contacts of Tetracycline* Proposed
a case

Contd...
 Rational Drug Therapy in Pediatric Practice 223

Contd...

Pathogen Disease to be prevented Antimicrobial Efficacy

agent

Treponema pallidium Syphilis in exposed persons Penicillin Established

Yersinia pestis Plague in household contacts Tetracycline or Proposed
or those exposed to sulfonamide
pneumonic disease
Parasites Overt infection (chloroquine Chloroquine Established
Plasmodium species sensitive) in endemic areas
(Malaria)
Pneumocystis carinii Pneumonia in compromised Trimethoprim- Established
host Sulfamethoxazole
Viruses Influenza in those risk of Amantadine Established
influenza A complications

*Not given to children younger than 9 years if acceptable alternative

drug is available Adopted from Report of the committee on infectious
diseases American Academy of Pediatrics Ed. 1991.

Choice of Antimicrobials with Dose and Duration (U or Mg/kg/day)

Category Drug of choice Neonate 8-28 days Infant/children

0-7 days

Streptococci
Group ‘A’ Penicillin G 100,000 U/6 hr 150,000 U/6 hr 250,000 U/4 hr or
Group ‘B’ Penicillin G 100,000 U/6 hr 6 hr
or 150,000 U/6 hr 250,000 U/4 hr or
Ampicillin 100 mg/12 hr 100-200 mg/8 6 hr
+ Amino 12 hr 100-200 mg/6-8 hr
Glycoside
Gentamycin 5-7 mg/12 hr 5-7 mg/hr 5-7 mg/12 hr

Group C & G Penicillin 100,000/12 hr 150,000/6 hr 250,000/4 hr or 6 hr

(Non group A
streptococci)
Group ‘D’
L mono- Ampicillin 100-150/12 hrs 150-200/8 hr or 200-300/6 hr
cytogens 6 hr

Coliform Ampicillin 15-20 mg/12 hr 150-200/8 hr 200-300/6 hr

group Gentamycin 5-7 mg/12 hr 7.5 mg/8 hr —
Chloram- 25 mg/12 hr 50 mg/8 hr —
phenicol

Pseudomonas Carbenicillin 200 mg/12 hr 300 mg/12 hr 125-150 mg/4 hr

Qeruginosa
Ceftazidime 50 mg/12 hr 90 mg/12 hr 125-150 mg/4 hr

Contd...
224 Selected Topics in Pediatrics for Practitioners

Contd...

Category Drug of choice Neonate 8-28 days Infant/children

0-7 days

H. influenzae B
- Betalactamase Ampicillin As above As above As above
negative strain
-Betalactamase Chloram- 60 mg/12 hr 90 mg/8 hr 125-150 mg/4 hr
positive strain phenicol
or cefotaxime 100 mg/12 hr 100 mg/8 hr 100-150 mg/6 hr

Pneumococci Penicillin G As above As above As above

(Strep. or Ampicillin
pneumoniae)
Meningococcus Penicillin G As above As above As above
or Ampicillin

Staphylococcus Methicillin 100-150 mg/12 hr 150/200 mg/8 hr 200 mg/6 hr

or or 8 hr or 6 hr
Vancomycin 20 mg/12 hr 30 mg/8 hr 40-60 mg/6 hr
Cloxacillin 25-50 mg/8 hr 25-50 mg/8 hr 50-100 mg/6 hr

Proteus Cefotaxime 25-80 mg/12 hr 150-200 mg/ 200 mg/6 hr

12 hr or 8 hr
Ampicillin and 100 mg/12 hr —do— —do—
Kanamycin

E. coli Cefotaxime 100 mg/12 hr 150-200 mg/8 hr 200 mg/6 hr

Ampicillin and —do— —do— —do—
Gentamycin —do— —do— —do—
Co-trimoxazole 20 mg TMP 20 mg TMP + 20 mg TMP +
I/V in excep- + 100 mg 100 mg 100 mg
tional case SMZ/6 hr SMZ/6 hr SMZ/6 hr

Salmonella Chloramphenicol 50-100 mg/6 hr for

typhi children
a. Conventional < 2 years
50-100/6 hr for
children > 2 years
Cotrimoxazole 12 mg/of TMP/
+ Furazolidone 12 hr
10 mg/12 hr
Cortimoxozole —do—
+ Cephalaxin 30-50 mg/6-8 hr

b. Multidrug Ciprofloxacin 10-15 mg/12 hr

resistant strain Ofloxacin 8-15 mg/12 hr

Judicious use of drugs/antimicrobial agents therefore depend on

variety of factors delineated above. It should be clearly emphasized
that over use/irrational use of fixed drug combination with reference to
dosage, frequency and duration against community/hospital acquired
infection in human is largely responsible for increase in their resistance.
 Rational Drug Therapy in Pediatric Practice 225

BIBILOGRAPHY
2. Desai AB et al. Immunity Immunization and Infectious Diseases: IAP Publication
1994;279-83.
1. Krishnamurthy PN. Rational drug therapy in acute lower respiratory tract
infection (LRTI) in childhood; Pedicon update, IAP Kannur. 2002;6-8.
3. MIMS India. In CM Gulhati (Ed): MIMS India Publications: New Delhi
2003;23(8):6,15.
 22
Pediatric Surgical Referrals
RK Bagdi

As practitioners of child health we must be aware how to identify and

refer pediatric surgical cases at the appropriate age. Pediatric Surgical
Referrals are made (a) for establishing diagnosis on clinical suspicion.
(b) following diagnosis made after imaging and (c) for surgical treatment
for elective and emergency surgical conditions. The Paediatric Surgeon
is also involved in decision making following intrauterine diagnosis of
an abnormal fetal scan done at 16-20 weeks of gestation. Long term
follow-up and repeated referrals are made to the paediatric surgeon in
treatment of children with deformities and tumors.
Delay in reaching the paediatric surgeon is mostly because of factors
relating to parental ignorance and rarely due to the pediatrician that
there is no delay in referral on his part. Hence he must acquire a good
knowledge of paediatric surgical entities and refer appropriately. All the
same paediatric surgeon should be also aware of medical illnesses
mimicking surgical emergencies and not be caught on the wrong foot.
Always be alert, broad minded and cautious in diagnosis.
For elective procedures some guidelines can be given on timing of
surgery. Here the safety of paediatric anaesthesia and freedom from
complications remain the prime concern to determine the age of surgery
most procedures today can be completed by one year of age.

Referral for Diagnosis

After exclusion of medical illness surgical referrals can be made for the
following symptoms.

Some Examples

S no. Symptoms Diagnosis

1. Vomiting non bilious, projectile Pyloric stenosis

2. Vomiting bilious with a scaphoid abdomen Malrotation
3. Vomiting bilious with bleeding per rectum Volvulus
4. Bleeding per rectum in an infant Intussusception

Contd...
 Pediatric Surgical Referrals 227

Contd...

S.no. Symptoms Diagnosis

5. Acute Scrotum Torsion testes

6. Ascites in new born Urinary ascites
7. Dribbling of urine Posterior urethral valve
8. Hematuria Wilms Tumor
9. Respiratory Distress Congenital
Lobar emplysema
Congenital.
Cystadenomatoid
malformation, congenital
diaphragmatic hernia
10. Cellulitis is in infancy Osteomyelitis

In most of these instances the pediatric radiologist is also involved

in the diagnosis. The surgical referral may be made before or after
establishing the diagnosis. However interventions, investigations and
procedures must be done with the involvement of the pediatric surgeon.

TIMING OF SURGERY
Surgical conditions can be classified into three categories according to
the degree of urgency with which treatment should carried out.
1. Emergency group-conditions where immediate operation is required.
2. Semi emergency group-where treatment is not urgent but should
never the less be undertaken without undue delay.
3. Elective group-where operation is performed at an optimum age
determined by one or more factors which affect the patients best
interests.

Emergency Group
Trauma, acute infections, Abdominal emergencies and Acute Scrotal
conditions fall under this category and in most cases immediate surgery
has to be done. An important sub group consists of Neonatal Emergencies.

Neonatal Emergencies
Most of these are the result of developmental abnormalities causing
disorders of functions. The best prognosis depends upon early diagnosis,
speedy transport to a hospital where appropriate skills and equipment
are available and effective surgical management. Some important
neonatal emergencies are:
1. Esophageal atresia
2. Imperforate anus and rectum
3. Neonatal intestinal obstruction
228 Selected Topics in Pediatrics for Practitioners

4. Diaphragmatic hernia
5. Lobar emphysema
6. Congenital cystic disease of the lungs
7. Pierre-Robin syndrome
8. Exomphalos
9. Tension pneumothorax
10. Myelomeningocele and meningocele.

Intermediate Group
This includes a variety of conditions, For examples:
1. Inguinal hernias, prone to strangulation. Hence, surgery should be
performed within few days of diagnosis.
2. Swelling or masses suspected to be malignant. Investigation of an
abdominal mass or excision biopsy of a superficial swelling.
Example In the neck. Should be undertaken within few days of its
discovery.

Elective Group
Factors which favor deferment of operation and hence may determine
an optimum age are.
The possibility of spontaneous correction or cure. In infants, congenital
hydrocele, umbilical hernias and sternomastoid tumors all show a strong
tendency to spontaneous resolution.
Hemangiomas though may progress in the first year of life, usually
close and fade spontaneously in ensuing 2-4 years. In general they should
be left alone to do so, for surgical measures are rarely required.
Hemangioma though may progress in the first year of life, usually
close and fade spontaneously in ensuing 2-4 years. In general they should
be left alone to do so, for surgical measures are rarely required.
1. Capacity for healing and adaptation in the very young. This can be
relied upon in many conditions.
2. Stimulation of development by early treatments is well shown in
infants with congenital dislocation of the hip.
3. Malleability of infantile tissues, an advantage for eg. in talipes, in
which the best results are obtained when treatment is commenced in
the first few days after birth.
4. Avoidance of undesirable psychological effects. These can be preven-
ted by completing treatment particularly repetitive painful procedures,
before the remembrance of things past is established or before the
child goes to school where obvious deformities are likely to attract
attention.
 Pediatric Surgical Referrals 229

Optimum Ages for Operation

Diagnosis Usual operation Optimum age for

Operation
operation

Emergency Group
Oesophageal atresia and Ligation of fistula and First day
tracheo-oesophageal fistula oesophageal anastomosis
Diaphragmatic hernia Laparotomy and reduction of
Hernia and repair
Hirschsprung’s disease I. Colostomy On diagnosis
II. Recto sigmoidectomy and
Pull through 9 months
or
Single stage surgery On diagnosis

Imperforate Anus and Rectum

Low anomaly Ano plasty Soon after birth

High anomaly I. Colostomy Soon after birth
II. Pull through 6 months
III. Closure of colostomy 9 months

Exomphalos

Minor-defect less than 5 cm Immediate complete repair On day of birth

Major-defect more than Staged approach
5 cm
Gastroschisis Immediate repair/silo if necessary On day of birth
Lobar emphysema and Lobectomy of the affected urgent
Congenital cystic disease Lobe

Semi Emergency Group

Inguinal hernia Herniotomy When diagnosed

CTEV Manipulation followed by Day one

splinting or plaster
Surgical correction 6 months
Congenital dislocation Bilateral abduction in Day of birth
of the hip flexion
Pyloric Stenosis Pyloromyotomy As soon as
diagnosed
Patent ductus arteriosus Closure of the ductus by ligation As soon as
convenient
Sacrococcygeal teratoma Excision Within a few days of
birth
Intersex Stage 1-investigations 1-2 days
Stage 2-feminizing
genitoplasty 6 months

Contd...
230 Selected Topics in Pediatrics for Practitioners

Contd...

Inguinal hernia Herniotomy When diagnosed

Gonadectomy 12 years
Meningocele Excision of sac & Closure 1-2 days
Myelomeningocele Stage 1-excision of sac & repair 1-2 day as
Stage 2-VP shunt if when diagnosed
Hydrocephalus develops
Hydronephrosis Pyeloplasty 3 months
Vesicoureteric reflux anti reflux procedure 6 months
Obstructive megaloureter reimplantation 6 months
Posterior urethral valves fulgration on diagnosis

Elective Group
Undescended testes Orchiopexy 15-18 months
Cleft lip Repair of lip 3 months
Cleft palate Palatoplasty 12-15 months
Hypospadias Correction in one or two stages 1-4 years
Umbilical Hernia Herniorrhaphy 2 years
Congenital Hydrocele Ligation PV sac 2 years
Branchial Sinus Excision tract 2 years
Thyroglossal Cyst Sistrunks operation 2 years
Tongue tie Tongue tie release 15 months
Torticollis Torticollis release 1 year
Biliary Atresia Operative cholangiogram and
Kasai operation 6 weeks
Ectopia Vesicae Stage 1-closure of bladder 1st week
Stage 2-repair of bladder neck 3 years
Stage 3-urethroplasty 4 years

BIBLIOGRAPHY
1. Pediatric Surgical Referrals-Guidelines’, Dr RK BAGDI, Pediatric Update-2003,
IAP Kancheepuram August 20:2003;60-64.
 23
Designing Medical Research
in Office Practice
N Deivanayagam

INTRODUCTION
Practice of clinical medicine is a combination of art (derived from the
beliefs, judgments, and intuitions we could not explain) and science
(derived from the knowledge, logic and prior experience we could
explain).
Understanding the fundamentals of medical research is essential in
decision making to solve problems encountered in clinical medicine in
patient care—etiology, diagnosis, treatment, prognosis and will help
clinicians to evaluate the constant flow of new medical information. The
basic purpose is to identify and apply methods in clinical observations
to reach valid conclusions. This knowledge is needed not only as a
“Doer” of research but as consumer of researches published. Critical
appraisal of clinical evidence in the published literature of health sciences
(on etiology, diagnosis, treatment, prognosis, etc.) is an important aspect
for every clinician. Understanding of research methodology is crucial
for critical appraisal.
POSSIBLE EXPLANATIONS FOR CLINICAL OBSERVATIONS
Bias
The observation is incorrect because a systematic error was introduced
by Selection bias—the method by which patients were selected for
observation. Measurement bias—the methods by which the observations
or measurement was made. Confounding bias—the presence of another
variable which accounts for the observation.
Chance
The observation is incorrect because of error arising from random
variation.
Truth
The observation is correct (accept this explanation only after excluding
the others).
232 Selected Topics in Pediatrics for Practitioners

It is aimed that the clinician should be able to recognize, avoid or

minimize bias. Clinical observation is valid if it corresponds to the true
state of affairs. If it has to be valid, it must neither be biased nor incorrect
due to chance.
It is true that the two well established places of research are the
community and the hospitals. The community research mainly involves
on incidence, prevalence, demography, implementation of health care
programs, community interventions, etiology/causation especially
environmental factors, life style features, etc. Research in hospitals are
mostly on tertiary care patients. Research on selected patients in a hospital
setting, a tertiary care setting, will not always be transferable into general
practice. Therefore, it is not only useful, but quite necessary to perform
research in general practice. What can the general practice researcher
add to the scientific community? The general practice research differs
from research on more selected patients in the hospitals. The general
practitioner makes the most of his/her unique position to do research
that is not possible in a hospital. He/she alone has the opportunity to
perform research on the common conditions. How often does a hospital
physician see patients with common colds, otitis, tonsillitis, cystitis,
tension headache, insomnia, moderate hypertension etc. The general
practitioner meets early and incomplete diseases. He/she follows the
patient throughout the process. This provides unique possibilities for
research on predictive and prognostic factors. Patients in a hospital have
passed through a filter, a referral filter. They are not representative for
the usual patient with otitis or hypertension. The selection mechanisms
are so strong that it is necessary to conduct new research in selected
areas of general practice. Guidelines developed in hospitals may be
even harmful if they are applied uncritically in general practice. A strong
selection process controls this stream of patients, and that fact should
entail consequences for the generalizability of research results. Some of
the research conducted in the university clinic may not be generalized
to general practice. Involvement by community physicians in practice-
based research has the potential to change the culture of primary care
in the community. However, we should also keep in mind that the help
seeking behavior in the population also constitutes a strong selection.
We cannot generalize findings in our own practice to the whole
population.
There are a few steps to be considered to design a study. These steps
can also be used to perform critical appraisal of a published paper.
Designing of a study for office practice is not different from that of
hospital or community. The use of these steps, a simple system, can
ensure that biases in study design are avoided.
 Designing Medical Research in Office Practice 233

The Research Question

The development of the hypothesis comes after you have had the idea
for the research. This is perhaps the most difficult of all the steps in
designing a study. Refine the hypothesis in a question form which will
include the following aspects.
i. One sentence in the form a question
ii. Is it important in terms of clinical significance?
iii. Is it possible/feasible to answer the question in general?
iv. The study population to be defined
v. The exposure or intervention is specified
vi. The endpoint of interest (primary outcome event) is specified in
quantifiable terms

Introduction
Explain why the idea is good (scientific rationale). Establish the basis for
hypothesis/question, selection of variables (outcome events), and cite
existing support for your study.

Review of the Literature

Establish what is already known and critically review the strengths and
limitations of evidence. Describe the methods you are going to use in
this study to overcome the limitations.

Objectives
Specify the driving force behind the research and also how the
investigation and conclusion shall help the patient management or health
care.
Study design Justify the choice, both scientific and practical. In the sample
specification, the issues to be considered are generalizability and internal
validity—whether the results of your study can be applied to other
populations. It has to be defined how the sample is selected for your
study—inclusion and exclusion criteria.

Sample Size
The factors to be considered are, the expected frequency of events in
control and study groups, clinical significance to interest, Type I and
Type II errors used in the calculation. It is essential to involve a statistician
in the beginning of the study itself.

Description of the Methods

How the study population is allocated to the groups. Generally a
randomization process is followed to eliminate bias. The methods must
234 Selected Topics in Pediatrics for Practitioners

be defined sufficiently and precisely to be reproduced, that is who does,

what, to whom, when and how. Indicate how compliance will be achieved
and assessed.

Outcome Measures (Variables)

The outcome measures are the study endpoints and reflect what we
want to achieve. Specify the outcome event being measured and how
it is measured. How harmful or adverse effects will be detected in case
of intervention?

Results and Analysis

Statistical analysis at various levels will be—Baseline data—characters
of subjects sampled and studied, Simple comparison of the groups;
Comparison with other variables taken into account; comparison with
simultaneous adjustment for multiple variables. Time schedule of the
study in the form of a diagram or a table is preferable incorporating the
schedule for completion of various components from proposal through
completion—protocol development, data collection and research review.
Ethical issues include review and approval by the ethics committee,
informed consent and termination policy. Some common study designs
are outlined below:

Randomized Controlled Clinical Trial (RCT)

An investigation in which assignment of patients to study groups is by
random allocation. The cohorts (2 or more groups) of individuals so
generated are and are not exposed to the experimental maneuver and
followed up for the outcome of interest. Comparisons are made at the
start and at the end of the study. The advantages of RCT is that by
randomization, the bias known and unknown, is likely to be equally
distributed between the groups.
An example of research question could be: Is Amoxycillin given
orally in a dose of 50 mg/kg/day in four divided dose is better than
Chloramphenicol in a dose of 100 mg/kg/day given in four divided
dose in clinical cure of Typhoid fever?

Cohort (Non-equivalent) Group Concurrent Study

An investigation in which the study groups are assembled according to
whether or not the exposure to the clinical maneuver or putative causal
factor has occurred. Exposure is not under the control of the investigator
and as a result study groups may not be comparable ( i.e., not equivalent)
on all important prognostic features. Outcome is not present at the time
 Designing Medical Research in Office Practice 235

sampling. This is most suitable to study the risk factor or cause for a
disease. An example of research question could be as above except
randomization, and instead alternate patient is allotted to the groups.

Case Control Study

An investigation in which patients with or without an outcome of interest
are selected and the investigator determines their prior exposure to the
putative cause or manoeuvre. This design is useful to identify the risk
factors or possible etiology in a short time.

Cross Sectional Survey

An investigation in which a single sample of people is drawn and
assessment of the whole cohort for exposure and the outcome of interest
is carried out at the same time. Several potential causal factors can be
compared with several outcomes. The investigator has no influence as
to which patients are exposed to the proposed casual factors or
interventions. It is useful only to generate hypotheses.

Descriptive Study
An investigation is carried out to provide descriptive data. There is no
control group for comparison. This could be done for patients with
outcome of interest: An investigation is carried out to provide descriptive
data about the frequency of exposure to proposed casual factors in
patients with the outcome of interest.

What are the Areas in Which Medical Research in Office Practice

can be done?
Demographics General Epidemiology of the disease—age, sex, educational
attainment, income, race, ethnicity, language, marital status, and others
Health related risk behaviors: life style pattern—tobacco use, exercise, diet,
helmet/seat belt use, nonprescribed drug use, alcohol use, high-risk
sexual exposures, and others.
Clinical—all the areas of research in a hospital settings, except perhaps
acute/emergency care, surgery—can be done at office practice.
A descriptive study of case report or better case series—identification
disease pattern, particularly when a new disease appears, an outbreak
of disease—signs and symptoms, course of the disease, prognosis, natural
course of the disease etiology or causation, particularly environmental
factors, diagnostic studies, preventive services—vaccination, disease
control, eradication programs.
236 Selected Topics in Pediatrics for Practitioners

Medical research at office practice can be done by a single individual,

by a group of practitioners of similar discipline or by Practice-Based
Research Networks (PBRNs). Practice-Based Research Networks are
based on the principle that the experience, wisdom, and insight of the
practicing physician are powerful tools for identifying and framing
research questions that are relevant to practice and improve the practice
of primary care medicine. The PBRNs link the relevant research questions
of the practicing physician with rigorous research methods to produce
research results that are in theory more easily assimilated into everyday
practice.
Research conceived and conducted in practice can follow a short
feedback loop back into practice. The PBRNs focus their activities on
practice-relevant research questions, apply appropriate research design,
and generally avoid the tendency to permit research methods to define
the question. Networks strive for the systematic involvement of network
clinicians in defining the research questions, participating in the study
design, and interpreting the results.

BIBLIOGRAPHY
1. Fletcher RH, Fletcher SW, Wagner EH. Clinical epidemiology—the essentials.
Baltimore: Williams and Wilkins, 1982.
2. Heller R. Designing a research study. Ind J Pediatr 2000;66:39-41.
3. P Nutting, J Beasley, J Werner. Practice-based research networks. JAMA 1999;281-
88.
4. Sackett DL Haynes RB, Tugwell P. Clinical epidemiology—A basic science for
clinical medicine. Toronto: Little Brown and Company, 1985.
 24
Childhood Communication
Disorders
Roopa Nagarajan

INTRODUCTION
The birth of a child is a significant event. Parents and the family monitor
the growth and development of the child with joy, anticipation and
excitement. The first smile, the first step and the first word uttered by
a child are often moments that remain etched in the minds of the parents
and family. The development of communication and speech is often
taken for granted until a breakdown occurs. Parents today seek profes-
sional help when they are concerned that their child is not speaking, the
child’s speech is not clear or the child is not hearing well. Doctors are
often the very first professionals to come in contact with a child with
a communicative disorder. It is important for this reason that medical
professionals, especially pediatricians should be sensitized towards
communicative disorders.
The pediatricians should not only be aware of the milestones in
communication development, but also causes, the effects, the signs and
symptoms of the delayed or disordered communication and recommend/
refer for appropriate investigations/intervention. Pediatricians also have
the important responsibility to prevent the development of communi-
cative disorders.
An impairment that is not corrected leads to a disability (limitation
of activity) and if ignored or uncorrected could result in handicap (limited
participation). This could happen irrespective of age of onset, severity
of disability and etiology. For example, a child with a moderate fluctu-
ating conductive hearing loss may behave like a child with a severe
disorder if the hearing loss is ignored. The impact of impairment is
influenced by age, gender, socioeconomic status, attitude of the
community and support facility available.
The term “communication disorder” is a broad label that includes
disorders of speech and language or both without reference to etiology.
Communication impairment could result because of a breakdown in
speech, language or hearing. One or all aspects may also be affected.
Just as a child with hearing loss may have a communication disorder,
238 Selected Topics in Pediatrics for Practitioners

so also a child with stuttering, cognitive deficits, autism, cerebral palsy

may also be categorized as having a communicative disorder.

Magnitude of the Problem

The National Survey Sample Organization (NSSO) in 1991 in a survey
estimated that 1.9 percent of India’s population had a disability. There
is not yet any no definitive estimate of the prevalence and incidence of
communicative disorders in India. It is expected that the latest census
should throw some light on the estimate of the disabled population. The
status report on disability in India 2000, has reported data with reference
to hearing impairment from various surveys and studies that included
the NSSO 47th Round, 1991, NSSO 1981 and 1996, WHO 1988 and 1998,
India Human Development Report 1999, ICMR multicentric study, 1983,
DRC Scheme, Proceedings of the Review Meeting, 1997 and studies by
individual researchers in urban and rural areas. The population included
in these studies ranged from general population as in Census and the
NSSO studies, school-going children-in rural and public schools, children
with learning disabilities, people with genetic hearing disabilities, those
with other deficiencies. The incidence figures have ranged from 0.4 to
75-88 percent. These studies are difficult to compare since they cover a
great variation in subjects, methodologies, and even the time frame in
which these studies were carried out.
Some of the following figures, are quoted in seminars and conferences
are based on small studies and unpublished data. About sixty children
are born deaf in India everyday. It is estimated that fifty percent of
sensory neural hearing losses are of genetic origin. About ten percent of
school-going children have some learning disability. About thirty five
percent of this learning disabled population would have central auditory
processing disorders. Approximately one in a hundred people stutter.
Approximately 35,000 children are born in India with a cleft lip and/
or palate every year.

Communication, Speech and Language

In order to understand communicative disorders, their nature and
management it is essential to have an overview of the normal communi-
cative processes. Most often, the terms communication, speech and
language are used interchangeably by the layperson. The communicative
process has three aspects—an input process (sensation, perception and
comprehension), an output process (formulation, motor planning and
motor control) and a common code (language) shared by the sender and
receiver. Impairment in either in the input processes (e.g. hearing
impairment) or output processes (e.g. stuttering) can have a devastating
 Childhood Communication Disorders 239

effect on communication. The impaired communication impacts learning,

education, social relationships and vocation. This has a profound effect
on the quality of life of the individual, his family and society.
The code used to transmit an idea from the speaker to a listener is
called language. Language is a socially shared code that represents ideas
through the use of arbitrary symbols and rules that govern the
combination of these symbols. Information can be conveyed from one
person to another through voice, posture, gestures or body language.
Speech, writing or sign language are modes of communication. Speech
is an oral verbal mode of communication. Language is conveyed from
speaker to listener through an oral to auditory path. The structures of
oral cavity and the vocal mechanism are used to modify the air stream
from the lungs to form individual sounds. These are combined to form
words and sentences. This spoken language received through the ears
is called audition or hearing. Therefore when language is presented
orally as speech, normal hearing is a prerequisite. It is through hearing
of language, that the sounds of speech, the accent, the rules of a language
and the patterns that are peculiar to a particular language are learnt.
This link between audition and language learning is a unique human
trait. Further this learning is time locked to early maturational periods
in life. Chomsky’s concept of critical period also apply to learning of
language. If auditory stimulation is delayed or absent, language learning
is less efficient/delayed/deviant.

Characteristics of Language
To be a communicative human being every child must acquire language.
All languages (socially shared codes) have five characteristics. They (i)
use arbitrary symbols, (ii) use a limited set of different fundamental
units, (iii) have vocabulary or lexicon, (iv) use a set of rules to link this
vocabulary together and (v) finally have a set of rules for using the
language in a social context. Language is generally viewed as consisting
of three major components form (structure), content (what to say) and
use (when to say).

Language

Form Content Use

Phonology Semantics Pragmatics
Morphology
Syntax
Prosody
240 Selected Topics in Pediatrics for Practitioners

The range and rules for using speech sounds in a language are called
phonology. The distinctive sounds of a language are called phonemes.
These phonemes are combined into meaningful units to develop the
vocabulary needed to communicate. The smallest meaningful unit in a
language is the morpheme. For example the/s/in the word books is a
meaningful unit in English that refers to plurality. Syntax refers to the
grammatical aspects of language -the word order, inflections and
relationships between words. The unique feature of every language is
its melody and rhythm, aspects that contribute to the prosody of a
language. This involves learning when to pause, how to use pitch
inflections, how to use stress and emphasis of syllables. Even before
children learn and use words and phrases, many language specific
prosodic patterns can be identified in the pitch inflections and intonations
in the speech of young children.
In order to communicate in a particular language one needs to know
how the phonemes and morphemes are combined to form words, phrases
and sentences. Word meaning represents the relationship between words
and the objects and the events they represent. This aspect of language
is called semantics. For utterances of words combined in an appropriate
grammatical sequence to constitute communication, it is necessary that
the speakers and the listeners observe rules of appropriate communicative
interaction. This is called pragmatics. An important component of
pragmatics is code switching where individuals can change speaking
style depending on how they interact with different listeners. While
learning of language occurs maximally in the early years, specific aspects
such as vocabulary learning, pragmatics, etc. continue life long.

Prerequisites for Normal Development of Speech and Language

Many disorders of communication have their onset very early in life and
over a period of time may result in delayed or deviant language and
speech. A speech pathologist evaluating a child would investigate if the
very basic conditions for normal speech and language development
have been met. Many disorders of communication have their onset very
early in life and over a period of time may result in delayed or deviant
language and speech. A speech pathologist evaluating a child would
investigate if the very basic prerequisites for normal speech and language
development have been met. For speech and language to develop
normally it is expected that i) the child’s vocal mechanism normal in
structure and function, ii) the child has normal hearing, intelligence,
cognition and neurological development, iii) the child has adequate
physical and emotional health to foster growth of language and iv) the
child’s environment conducive for (nurturing and stimulating) language
development.
 Childhood Communication Disorders 241

According to Van Riper and Eriksson (1996) three environmental

factors are crucial for speech development i) bonding with a caregiver
who provides reinforcement for communication, ii) at least one speech
model to use a simple but well formed language pattern, iii) opportunities
for exploration and day-to-day experience that stimulates the need to
communicate.

Milestones in Speech and Language Development

When a child is born with normal hearing and has a nurturing environ-
ment, he systematically acquires language and communication. As early
as the first trimester of gestation, responses to sound have been reported.
Parents automatically use slower rate of speech, use simpler sentences,
many repetitions and exaggerated stress while speaking to children.
This child- centered speech is called ‘motherese”. Some researchers believe
that this type of speech helps the young child in understanding the
communicative code. Normal audition and listening seems to be critical
and it has been reported that children with hearing impairment may
show delay or nondevelopment of canonical babbling.
Table 24.1 shows some typical stages in the development of speech
and language between birth and thirty months.
Table 24.1: Development of speech and language *
Age Communicative behavior

1-3 months Little sign of speech comprehension, Much crying. May cry differently in
expressing pain, hunger, or need for attention. Produces cooing and comfort
sounds. Does show response to sounds and moving objects.
3-6 months Seems to pay attention to the speech of others and to react to it. Less
crying and more cooing and the beginning of babbling. Responds to parental
speech and behavior by vocalization and imitation.
6-9 months Marked increase in babbling and word play. Vocal play shows inflections.
Comprehends certain words such as “Eat” or “Up.” Uses signs and some
syllables to express wants.
9-12 months Comprehends a few words and even phrases: “No” “Daddy come”. “All
gone.” “Go car.” Crude imitation of parent’s speech. Practises syllable
strings.
12-15 months Appearance of first words, usually monosyllables or repeated syllables: “
“Mama,” “Bye-bye,” “No.” Much jargon and self talk. Can point to objects,
toys, animals. Understands simple directions and the word “NO”. Has a
speaking vocabulary of six to eight words.
15-20 months Seems to understand most of what is said, if said simply. Regularly uses
words and short phrases to express desires. Imitates environmental noises.
Much self talk when alone. Begins to combine several words into primitive
sentences: “Eat all done.” “More milk.”
20–30 months Comprehends most adults if they speak slowly and simply. Knows names
of all familiar objects and activities. Speaks in phrases and sentences. Has
a vocabulary of about 100 words.

Adapted from Speech correction—an introduction to speech pathology and audiology Van
Riper C and Erickson RL (1996).
242 Selected Topics in Pediatrics for Practitioners

Speech and Language Disorders

The most classic definition of a speech disorder was given by Van Riper
and Eriksson (1996). They define speech as impaired when it deviates
so far from a speech of others that i) it calls attention to oneself, ii)
interferes with communication, and iii) causes distress in the speaker or
listener.
A speech pathologist goes beyond just identifying the presence of a
disorder. The manner in which the communication is impaired and
probable cause/maintaining factors would be explored. Assessment of
hearing is also a component of communicative evaluation. Each of these
aspects has an acceptable range of normality and differences. When
speech and/or language are impaired, there may be a deviancy in one
or more of the above components. It is also essential to identify the
elements that makes the speech conspicuous, hard to understand and
unpleasant. For example, a child with cleft palate may have a disorder
of resonance as well as articulation contributing to speech that is not
intelligible.
Disorders of communication are normally classified into disorders of
articulation, voice and resonance, fluency or language. For the purposes
of this chapter speech disorders involving articulation, fluency and voice
are discussed first followed by language disorders. A section on hearing
disorders is also included.

Articulation Disorders
A child with an articulation disorder has not mastered the speech sounds
of his language. There is some individual variation in the ages at which
children acquire these sounds. There is however a pattern in the acquisi-
tion of sounds. It seems children master labials, nasals, stop consonants
and glides first. This is followed by fricatives and affricates. Table II lists
the order and expected ages for acquisition of sounds of English. Most
children while learning speech show typical articulatory errors. It is not
uncommon for a child to say/l/for/r/or to lisp. Parents often describe
the speech of such children as persistence of “baby talk”. Some children
persist with these articulatory errors or are unable to produce it correctly
even past the age where it is expected to be mastered.
Articulatory disorders are normally categorized into two broad
categories—phonetic disorders and Phonological disorders. Individuals
with phonetic disorders are unable to produce sounds correctly because
of structural, motor, sensory impairment or organic abnormalities that
limit the speaking capability. Children with hearing impairment, a tongue
tie or a cleft palate have phonetic disorders. A child with a phonological
disorder is distinctively different from a child with a phonetic disorder.
 Childhood Communication Disorders 243

Table 24.2: Expected ages for development of speech sounds*

Expected age Sounds

< 3 years /p/,/b/, /m/,/t/,/d/,/n/,/w/,/h/. vowels

3-3½ years /k/,/g/,/ng/,/f/,/y/
3 ½-4 years /s/,/z/
4-4½ years /sh/,/l/, s-blends,l-blends
4½-5 years /ch/,/j/, lateral lisps
5 < years /r/,/v/,/th/, r-blends, frontal lisps

*Adapted from Developmental Normative Scale developed by York Preschool Speech and
Language programs. www.beyondwords.com.

Though they can produce the sounds, they seem to simplify adult patterns
or have their peculiar patterns. An analysis of the sound errors will
reveal an underlying system of rules of how they organize their
phonemes. As they develop language and speech these phonological
patterns disappear. The phonological processes seen in children are
classified into syllable structure processes, assimilation processes,
substitution processes and voicing processes. Table 24.3 describes some
common phonological processes seen in children developing speech
normally. Some children persist with these patterns and are described
as having phonological disorders. Children may have both phonological
and phonetic disorders coexist.

Table 24.3: Common phonological processes seen in normally developing children

Speaking English

Syllable structure processes Final consonant deletion

Unstressed syllable deletion
Cluster reduction
Reduplication
Assimilation processes Velar assimilation
Labial assimilation
Nasal assimilation
Substitution process Gliding of liquids
Velar fronting
Voicing process Prevocalic voicing
Final devoicing

Articulation disorders are often described by the type of errors made,

i.e. substitution, omission, distortion or additions. The severity of the
articulation disorder is dependent on the number of sounds that are
misarticulated, their frequency of occurrence in the language, the type
and consistency of error patterns, and the stimulability of the child.
Misarticulation in speech can cause a great deal of difficulty in
communication and influence the intelligibility of speech.
244 Selected Topics in Pediatrics for Practitioners

Assessment includes a detailed history, a hearing screening, and a

thorough oral peripheral examination to assess the structure and
functioning of the organs of articulation. A language assessment is also
a part of this comprehensive evaluation. The assessment of articulation
is done through the administration of formal tests, and/or observation
of the child’s spontaneous speech. The speech pathologist would analyze
the type of errors, the patterns of errors, the factors (sensory, motor)
contributing to the errors, the stimulability of the child, and differentiate
between errors that are phonological and errors that are phonetic. Since
some sounds are acquired earlier and some sounds acquired much later,
the information has to be interpreted with reference to the age and
developmental level of the child.
Developmental apraxia of speech is a disorder of articulation charac-
terized by difficulty with sequencing and organizing motor or muscle
movements specifically for the production of speech. Muscle weakness
is not associated with developmental apraxia. This is a subgroup of
disorders often referred to as motor speech disorders. These children
have difficulty in sequencing the movements of articulators and to
produce may have dysarthria. The type of dysarthria is dependent on
the underlying neurological status of the child.
Intervention in children with articulatory disorders is planned based
on the possible etiology, a careful analysis of the error patterns and the
developmental level of the child. Common sub-goals in all articulation
therapy are i) sensorimotor training to help a child become aware of his
errors, ii) facilitating production of the target sound iii) stabilization of
the use of the sound in a variety of contexts and finally iv) the carry
over/transfer of the sound to spontaneous speech. Children with
dysarthria require different techniques and would benefit with a team
approach. The therapy approaches for developmental apraxia also differ
from traditional articulation therapy for children with phonetic/
phonological disorders. There are children with very severe communi-
cative dysfunctions such as some children with cerebral palsy showing
dysarthria and children with developmental apraxia, where oral
communication is not a realistic option. These children and their families
need to be counseled to consider other communicative options such as
augmentative and alternative communication devices to facilitate
expressive communication. In the past few years this has become accep-
table form of communication for those who are limited in their ability
to use speech for expressive communication.

Fluency Disorders
The most commonly seen fluency disorder in children is stuttering where
speech habitually shows interruptions in the form of hesitations,
 Childhood Communication Disorders 245

repetitions or prolongations. Most individuals who stutter can speak

perfectly when they sing or when they are alone.
Stuttering varies with situations and usually increases when there is
fear or shame. Therefore stuttering is often interpreted as a communi-
cation disorder rather than a speech disorder. It is not uncommon for
a child between the age of two and four (when the child is mastering
fine motor speech skills and learning language) to exhibit stuttering like
behavior but be unaware of his disfluencies. This condition is described
as normal dysfluency. Some children do not outgrow their disfluencies
and this is characterized as stuttering. As disfluencies increase, frustration
sets in and the child begins to struggle. A speech pathologist would
analyze the child’s speech to assess if the child is likely to outgrow the
disfluencies (i.e. have normal non-fluency) or will benefit with
intervention (i.e. child has a stuttering pattern). The assessment protocol
for children with disfluencies includes analyzing the type of speech
patterns, the visible or audible manifestation of the problems, strategies
the child uses to avoid or postpone the speech attempt and the child
does to release himself from the blocks in speech. The major differences
between the speech of normally disfluent children and children with
stuttering are contrasted in Table 24.4. These pointers are often used for
identifying children who will require support and intervention.

Table 24.4: Symptoms associated with normal dysfluencies and stuttering

Normal dysfluency Stuttering

Word/phrase repetitions present Syllable/sound repetitions present

Sentence repetition present Sound prolongation present
Hesitation and interjection present Sound blocks present
No awareness Aware of his speech
No secondaries seen Secondaries noticed
No avoidance behavior Avoidance behavior present

The management of a child with stuttering is challenging and

multifaceted. Intervention strategies would depend on age, the severity,
and the presenting symptoms. It is accepted that earlier the problem is
identified and intervention begun, the more is the likelihood of successful
outcome.
Cluttering is also classified as a fluency disorder. It is distinct from
stuttering in that while there are breaks in speech, the person who
clutters repeat words, show no fear of words or situations and have little
awareness of their speech disruptions. The very rapid rate of speech
makes their speech unintelligible. Speech sounds or syllables may be
omitted. Some researchers suggest that cluttering is a symptom of
learning disability because many people who clutter often have difficulty
in reading, writing and spelling.
246 Selected Topics in Pediatrics for Practitioners

Voice Disorders
The first cry at birth is probably the most dramatic use of voice an
individual will ever make. It signals that the infant is alive and respiration
has commenced. The pitch is extremely high (approx 400-500 Hz—
above the adult male habitual frequency) and a periodic with hypernasal
resonance. As the child grows older, the pitch reduces in both the boys
and girls. However, the distinction in voice (pitch) across gender is
noticeable only during the pubertal age. During puberty (13-14 yrs) due
to the endocranial changes, the larynx becomes larger, the vocal folds
become longer and the pitch lowers by 1-1½ octaves in boys and it
reduces by less than ½ octave in girls. This sudden lowering of pitch in
boys accompanied with unclear, rough voice with pitch breaks is often
called stormy voice mutation. When boys resent this change in voice
due to psychological reasons and peer pressure, the result is a mutational
falsetto called ‘puberphonia’. This can best be treated by symptomatic
voice therapy. The voice stabilizes in men by the age 17-18 yrs. The
normal Indian adult male habitual frequency is 80-180 Hz and 180-280
Hz in case of Indian adult female.
Voice disorders include disorders of pitch, loudness and quality.
Disorders of voice can be caused by structural abnormalities, neurological
and physiological conditions and may have a psychological origin. The
most common causes for voice disorders in children are abuse, vocal
allergy, nonmalignant growth and some neurological conditions. It is
important to carefully evaluate the medical, neurological and
psychological factors.
Disorders of resonance: Normal speech requires the coupling of the
nasal and oral cavities. This is regulated by the velo-pharyngeal port.
The closure of the port allows for separation of the oral and nasal
cavities and permits the production of non-nasal consonants and vowels.
A resonance disorder occurs when there is a velo-pharyngeal dysfunction.
Hypernasality is a feature of velo-pharyngeal dysfunction and may have
an anatomical or physiological cause. Nasal air emission can be in
addition to the hypernasality when there is a velo-pharyngeal dysfunc-
tion. Nasal air emission occurs on the production of pressure consonants
while hypernasality is due to the improper velo-pharyngeal seal during
the production of vowels. This condition is often seen with children cleft
palate and submucous clefts. Hyponasality occurs when there is
decreased coupling between the oral and nasal tract and usually has an
anatomical cause. A significant obstruction of the nasal cavity, improper
velar timing or adenoids could all result in hyponasality.
 Childhood Communication Disorders 247

Language Disorders
Language disorders are the most devastating of communication
impairments because they affect the very substance of message i.e. the
code or symbol. In some cases, specific causes can be identified for
language impairment. Hearing loss, cognitive deficits, brain injury,
emotional problems, illness and or lack of stimulation in early childhood
years are conditions that could manifest in disorders of language.
Language disorders range from mild disturbance to profound or
total absence of language. Some children born with genetic conditions,
illnesses or other disabilities could have some conditions that interfere
with their language development. Children with hearing loss, cleft palate
and cerebral palsy are considered at higher risk for developing language
disorders. Children who are frequently hospitalized, those with low
birth weight are at increased risk for language learning difficulties. The
significant factor here is the lack of stimulation and the limited
opportunities the child has to explore and interact with people around.
In such cases, parent counseling, early intervention and integrating
intervention with other management such as - medical treatment, physical
and occupation therapy is needed. Late talkers are also at significant
risk for developing language disorders. They are slow to acquire the
first words and are slow to combine words into sentences. It is important
to monitor these late talkers as they go into schools because they are
often at risk for learning disabilities. Some children with cognitive deficits
never learn the rules of language and their vocalizations are limited and
meaningless. Others such as the deaf may acquire language, but however
use a different mode such as sign language to communicate.
Most speech pathologists differentiate between delayed and deviant
language. A child with delayed language shows functioning that would
be considered normal at an earlier age or their language skills are not
developed as expected given their age. Even though a child with delayed
language development could also show many articulatory errors the
real difficulty lies in the underlying language concepts. Children with
deviant language do not show linguistic patterns that are seen in the
normal language development but they use forms that are atypical.

Developmental Language Disorders

Some children with normal cognitive abilities, normal hearing, and no
disease or conditions that puts them at risk for delayed language
development still show language impairment. These children lag behind
their peers in language skills. Altered brain development is suspected
in these children who, demonstrate atypical language development.
These children could have difficulties in reception or expression of
248 Selected Topics in Pediatrics for Practitioners

language or both. When such deficits occur without any other known
causes, the child is said to have “Specific Language Impairment”. Some
of these children do achieve parity with their normally developing peers
but others continue to lag behind.

Disorders that Impact Language

Attention deficit disorders (ADD) are characterized by inattention and
impulsivity and hyperactivity (in a small group of children). Their
primary difficulty is in focusing and sustaining attention. These children
have a significant handicap in the classroom where they have difficulty
listening to directions and completing work. A subset of children with
ADD have speech and language problems that may be independent of
their attention problem. Therefore audiologist and speech pathologists
are often on teams that assess and provide intervention for these children.
ADD is usually managed medically and behaviorally.
Pervasive developmental disorders (PDD) is a generic term referring to
a group of disorders that are characterized by impairments in social
interaction, impairments in verbal and nonverbal communication and
restrictive, stereotypic patterns of behavior. There is considerable
variability in symptoms and severity among individuals with PDD.
Conditions such as Autism, Asperger’s Syndrome, Rett’s Syndrome, etc.
are usually included in this category.
Autism spectrum disorders profoundly affect the child’s interaction
with others. Not all autistic children have cognitive deficits and as these
children grow, their disturbed communication becomes apparent. Some
children acquire language and then lose it in the preschool years. For
others development is disturbed from the start. Poor language
comprehension and pragmatic skills are evident in most children. In the
most severe of cases, they have complete lack of speech and could be
mute. These children often have a disturbance in language use
(pragmatics). These children may often repeat words they just heard
(echolalia), use stereotyped speech and have disturbed prosody.
Childhood aphasia is seen in children who lose normally learnt language
skills because of brain damage. This may happen in conditions such as
infectious disease, tumors or seizures involving the brain. Many of these
children recover to have adequate language. Some use simple linguistic
structures such as short simple phrases and sentences. Their more difficult
problems seem to be related to reading and writing and following
directions.
Traumatic brain injury (TBI) can be as focal as a gunshot wound or
diffused as in head injury. This usually involves some injury due to
brain moving within the skull and contusions where the brain contacts
the skull. Children with language disorders consequent to TBI are quite
 Childhood Communication Disorders 249

a variable group. They differ from other children who have

developmental language disorders. This is because considerable learning
of language would have occurred before the brain injury. More often
than not, it is on the more complex language tasks such as a discourse,
planning and organization, regulating one’s own behavior where these
children show the greatest differences. Children with mental
subnormality have deficits in cognitive development and social adaptive
skills. Language development is very dependent on these very aspects.
The language correlates of children with mental sub-normality varies
depending on the severity of the cognitive deficits and also on the
conditions/syndromes that are associated with the subnormality.
Children with Down’s syndrome are quite different in their language
skills from other children. These children are slow in developing
communication. It is reported that they usually have more difficulty
with syntax and morphology of a language. The goal of providing
intervention to children with mental subnormality is to develop
communication skills to the limits of their cognitive and social adaptive
potential.
The term learning disability describes a neurobiological disorder in
which a person’s brain works or is structured differently. Learning
disabilities can affect a person’s ability to speak, listen, read, write, spell,
reason, recall, organize information, and do mathematics. The disability
can be described as having some deficits in core elements such as
attention, memory, perception, sequencing and language associated
elements such as deficits in reading, writing, mathematical concepts and
listening. A child with a learning disability is usually a child who learns
differently. Children with learning disabilities should not be confused
with individuals who have other disabilities such as mental subnormality,
autism, deafness, blindness, and behavioral disorders or those who have
had lack of educational opportunities. Children with attention disorders,
such as Attention Deficit/Hyperactivity Disorder (ADHD) may also
have learning disability. Diagnosis of learning disabilities is made using
standardized tests that compare the child’s ability to normal development
for a person of that age and intelligence. Special attention is given to the
time at which skills emerge, sequence within which skills emerge, the
quality of skill level and how it contributes to children’s functioning.
Care should be taken to distinguish between skills that are slow in
emerging and those that are different in quality, form and function.
Children with learning disabilities can and should be identified early
if possible even before a child goes to school. Current research indicates
that subtle or obvious speech and language problems are often the
earliest indicators of a learning disability. These may include delayed
speech and language development, word finding problems, persisting
250 Selected Topics in Pediatrics for Practitioners

phonological problems, immature syntactic development, perceptual

memory deficits, sequencing difficulties. Some common signs of learning
disabilities are listed in Table 24.5. It is obvious that with increasing age
the primary learning difficulty becomes a predominantly academic/
social/vocational problem. Children with learning disability benefit with
remediation and development of skills to compensate for their limitations.
Table 24.5: Common signs seen in children with learning disabilities

Preschool Kindergarten—4th grade

Speaks later than most children Slow to learn the connection between letters
Pronunciation problems and sounds
Slow vocabulary growth, often unable Transposes number sequences and confuses
to find the right word arithmetic signs(+,-,x,/,=)
Difficulty rhyming words Slow to learn new skills, relies heavily on
Trouble learning numbers, alphabet, days memorization
of the week, colors, shapes
Extremely restless and easily distracted
Trouble interacting with peers
Difficulty following directions or routines
Fine motor skills slow to develop

Grades 5th -8th grade High school students and adults

Reverses letter sequences (saw/was, left/felt) Continues to spell incorrectly, frequently

Slow to learn prefixes, suffixes, root words, spells the same word differently in a single
and other spelling strategies piece of writing
Avoids reading aloud Avoids reading and writing tasks
Trouble with word problems Has trouble summarizing and trouble with
Difficulty with handwriting open-ended questions on tests
Awkward, fist-like, or tight pencil grip Works slowly and has poor grasp of abstract
Avoids writing compositions concepts
Difficulty making friends
Trouble understanding body language and
facial expressions.

Assessment of Language Disorders

A detailed language evaluation usually covers four main areas i) a
detailed case history with the parent or caregiver as the informant, ii)
informal observation and elicitation of samples of the child’s
communication, iii) an assessment of a child’s receptive and expressive
language through formal and/or informal tests, iv) an evaluation of the
factors that are contributing to the language development (cognitive
evaluation, medical review, hearing assessment, etc.). In a country like
India where most people may be multilingual, the assessment of language
skills is especially challenging. The influence of the first language on
second language acquisition is an area of current research among langu-
age scientists.
There are many formal measures to assess language that are very
focused. A criterion reference measure is used to verify if the child can
 Childhood Communication Disorders 251

use a particular structure in different tasks. While a norm referenced

measure would be used to compare a child with other children of similar
age. Especially in India, where standardized language evaluation tools
may not be available in all languages nonstandard assessments become
very essential. Language evaluation should not be based purely on
history, observation or formal evaluation. Ideally, a combination of all
of the above is essential for a proper assessment and interpretation.

Language Intervention
Intervention is primarily aimed at facilitating language learning. It is
generally well accepted that early identification and early intervention
particularly through empowering parents seems to promote language
development. Certain techniques for speech and language stimulation
are advocated which include -modeling, expansions, extensions, parallel
talk etc. Pragmatic approaches to intervention feature process oriented,
child directed methods in naturalistic environments with self reinforcing
rewards. An eclectic approach towards language intervention is probably
most advocated.

Hearing Disorders
As discussed earlier, hearing is an important component of the
communicative process. The relation between hearing and the language
comprehension is described in Table 24.6. The human ear in its anatomy
and physiology seems to be specially adapted to receive and process
speech.
Table 24.6: Relationship between hearing and language comprehension

Age Hearing and understanding

0-3 months Responds to sounds by ceasing activity

Most responsive to speech
Low-frequency sounds inhibit distress, increase motor activity
High-frequency sounds increase distress, inhibit motor activity
4-7 months Responds to noise and voice by turning head to locate source
Distinguishes between friendly and angry talk
Listens to own voice
9-12 months Vocalizes in response to adult speech
Responds to name
“Listens” to people speaking
Responds to simple commands:
“Want more milk?” “Give it (an object) to me”; “No-no!” (some times)
18 months Comprehends up to 50 words
Enjoys nursery rhymes, songs
Points to pictures when named
Recognizes names of family members, pets, objects
Points to body parts (2-4) when named

Contd...
252 Selected Topics in Pediatrics for Practitioners

Contd...

Age Hearing and understanding

2 years Listens to stories read and wants them repeated over and over
Comprehends up to 1,000 words; figures out meaning by how words are
used in sentence
Follows two-step directions
Distinguishes one from many
Comprehends prepositions “in” and “under”
2½-3 years Listens to longer, more complex stores
Identifies action (“running,” “swinging”) in pictures
Comprehends 2,000-3,000 words
Understands some opposites (“go-stop,” “give-take,” “push-pull”)
Understands past and future
4 years Follows three-step directions with objects, pictures
Has number concepts to 3, 4
Identifies several colors
Understands most of what is said to him or her

From Speech Correction—An introduction to Speech Pathology and Audiology Van Riper C
and Erickson RL ( 1996).

The external and the middle ear are generally considered to be the
conductive mechanism. The inner ear (cochlea) and the auditory nerve
are the sensory and neural components of the peripheral auditory system.
Sounds reach the sensory elements (i.e. the hair cells in the cochlea)
through two modes- air conduction and bone conduction. For hearing
through air conduction to take place, sounds picked up by the pinna
travel to the inner ear through the external auditory canal, the tympanic
membrane, the ossicles in the middle ear cavity to the oval window.
From there the mechanical vibration is transmitted through the fluids
of the inner ear to the organ of corti, the sensory end-organ receptor for
hearing. Bone conduction hearing occurs when sound is transmitted
directly to the cochlea through vibration of the skull.

Classification of Hearing Loss

Hearing losses are generally categorized as conductive (involving the
external and middle ear), sensorineural (involving the cochlea and/or
auditory nerve) and as mixed hearing loss when there is a combination
of conductive and sensorineural components. If there is normal peripheral
function and auditory dysfunction can be demonstrated the hearing loss
is categorized as central auditory dysfunction.
Conductive loss occurs because of interference in the transmission of
sound from the external ear to the inner ear. In an audiogram this is
evident by normal hearing through bone conduction and poorer hearing
through air conduction. Once the sound reaches the inner ear when
loudness is increased the person is able to hear adequately. Conditions
 Childhood Communication Disorders 253

such as atresia, stenosis, wax in the ear, ossicular discontinuity result in

a maximum of 60dB air conduction hearing loss. Other conditions such
as middle ear effusion, otitis media, eustachian tube dysfunctions could
also result in significant amounts of conductive hearing loss. Many
syndromes especially associated with craniofacial malformations also
could have external or middle ear abnormalities resulting in conductive
hearing loss. Children with conductive hearing loss should be identified
early and monitored carefully and regularly. It is also essential that
appropriate medical or surgical intervention is explored when indicated.
Sensorineural hearing loss occurs when the sensory end organ that
is the cochlea and/or the neuronal pathway of the auditory nerve is
involved. Since the cochlea and/or the auditory nerve is affected, poorer
than normal auditory thresholds for hearing both through air and bone
conduction are evident. There is no more than 10 dB difference between
the air and bone conduction thresholds. It is important not to overlook
during physical evaluation of a child the possibility of sensory-neural
hearing loss because the external ear or middle ear appear normal.
Children could also have progressive hearing losses related to metabolic
diseases, systemic infections and hereditary conditions. Sensory neural
hearing losses are generally irreversible.
Mixed hearing loss results when both sensorineural and conductive
components are evident in the hearing loss. In these cases the bone
conduction thresholds are poorer than normal and air conduction
thresholds are even below that. The significant air bone gap would
indicate the conductive component in the hearing loss.
Children with central auditory dysfunction (CAD or CAPD) have
near normal auditory thresholds but have difficulty in understanding or
recognizing speech. It has been reported that as much as 35 percent of
children with learning disabilities may have central auditory processing
disorders. CAPD is a subtle disorder and it is important to be able to
identify these children. Some have a significant history of chronic otitis
media that has been treated or resolved. Their responses to sound are
inconsistent and some are unusually intolerant to very loud sounds.
Many have poor listening skills especially in the presence of noise. They
are poor in following verbal instructions especially complicated verbal
commands and may have difficulty with auditory localization skills.
Some have difficulty relating what is heard to the words seen on paper.
They may be unable to appreciate jokes, puns, or other humorous twists
of language. Children with CAPD are often identified after they reach
school as it is in learning at school their problems are highlighted.
Sophisticated electrophysiological and behavioral tools are available that
help to identify the specific difficulties in processing that these children
254 Selected Topics in Pediatrics for Practitioners

have. Remedial measures are also based on a detailed assessment and

are individualized.
Hearing loss is also described with reference to the degree of loss.
The degree of hearing loss also effects the ability of the child to learn
language and communicate.
Children with mild hearing loss (26-40 dB HL) have only a mild effect/
delay in language learning and some mild speech problems.
Children with moderate and moderately-severe hearing loss (46-70 dB HL)
miss a lot of conversational speech and do benefit with the help of
hearing aids/amplification. These children hear vowels are better than
consonants. Short unstressed words such as prepositions, word endings
are difficult for these children. This may lead to confusion in learning
meaning of sounds, confusion with grammatical rules, omission of words
and some misarticulations in speech.
Children with severe hearing loss (70-90 dB HL) find it difficult to learn
speech and language spontaneously. With early identification, fitting of
amplification devices and special education they can be benefited.
Without amplification they hear only their own voices, very loud speech
and environmental sounds.
Children with profound hearing losses (losses greater than 90 dB HL) need
intensive special education and their hearing even with amplification
may be limited. Many of these children supplement amplification with
speech reading. These children commonly have disorders of articulation,
resonance, prosody, giving their voice monotonous quality and abnormal
patterns. For many children with severe to profound hearing loss, the
learning of sign language as a mode of communication is becoming a
reality. Cochlear implants are also becoming a choice for children with
hearing impairment who are not benefited with a hearing aid.
The effect of hearing loss depends on the type and degree, age of
onset and configuration and etiology. The age of onset is important
because the effect of hearing loss is generally less severe in a child who
has post-lingual deafness (i.e. deafness acquired after the child has learnt
language) than a child who has pre lingual deafness (deafness acquired
before learning language). The perlingually deaf child is generally more
affected because he has an inadequate auditory input in the crucial
language learning years. The term hearing impaired is usually used with
children who can make some use of audition and the term deaf is used
for those who cannot benefit or who cannot use audition.

Early Identification of Hearing Loss

Hearing loss is a silent hidden handicap because children especially
infants cannot tell that they are not hearing. There is evidence that very
early identification of hearing loss and early intervention can prevent
 Childhood Communication Disorders 255

many effects of handicapping hearing loss such as delayed speech and

language development, social and emotional problem and poor academic
achievement. There is, therefore ample justification for early identification
of hearing impairment. Recognizing the urgency and importance of
early identification and intervention in the United States of America,
screening of all neonates is mandatory.
Early identification programs can be initiated at several levels.
Obviously the earliest identification should focus on newborns. Hearing
loss that is present at the time of birth is usually due to due to genetic,
intrauterine and perinatal factors. The auditory system, specifically the
cochlea, reaches its adult status by the gestational age of six months.
Currently, sophisticated tools such as the OAE (otacoustic emissions),
ERA (evoked response audiometry), ASSR (auditory steady state
response) allow for assessment of the auditory system at birth. Screening
of newborns must be noninvasive, quick and must be free from the
effects of environmental factors.
Universal screening programs especially with tools such as the ERA
and OAEs are expensive and not possible or feasible in our country.
Hence the high risk checklist has been developed and utilized to identify
those children who should be monitored further or referred for further
evaluation. It has been reported that the high risk checklist identifies
only about 50 percent of children with congenital hearing losses. Even
identifying those 50 percent would be important and cost effective. In
the US. The Joint Committee on Infant Hearing Screening (JCIH) (1994)
in its position statement has recommended the employment of high risk
register (HRR) only if universal newborn hearing screening (UNHS)
using ERA or OAEs is not available. The use of the HRR is reported to
help in the earlier identification of hearing loss in children with mild
and moderate hearing impairment. Other techniques such as behavioral
screening of newborns have their limitations.
Once leaving the hospital, the next opportunity for screening and
early identification takes place in well baby clinics, nurseries, immuni-
zation centers, and schools. These centers could also follow up children
with high risk factors such as family history of hearing loss and cranio-
facial anomalies. For these programs to be successful there has to be a
team approach. The physician, the pediatrician, the ENT surgeon have
a role to play.

Confirmation of Hearing Loss

The children who fail the screening must have a follow up and complete
audiological workup. To confirm the loss, audiological evaluations must
include behavioral measures and electrophysiological measures. The
tests used to confirm hearing loss should be able to provide ear-specific
256 Selected Topics in Pediatrics for Practitioners

information of the type and degree of hearing loss as a guide for planning
intervention.
The ideal test battery for very young infants should include a case
history of the child and the family, followed by electro physiological
measures of threshold such as ERA, OAE measurements, information
on the middle ear function, acoustic reflex threshold and observation of
behavioral response to sound. It is important to include a detailed
assessment of the child’s speech and language development and auditory
behavior. Today, ERA has become routine and the first choice in most
urban centers sometimes to the exclusion of behavioral testing and
detailed workup. OAEs are available in limited centers. Obtaining ear-
specific responses often has to wait until the child is older to be able to
participate in audiometry especially in centres not geared up to test the
pediatric population.
Childhood is a period when the children are prone to diseases known
to cause hearing loss. Most of the learning in the classroom takes place
through hearing. Of particular concern in school age are middle ear
pathologies that may result in conductive hearing loss. While school
health programs often include screening of vision, dentition and skin,
screening of hearing is seldom included. A large number of children
have impacted wax in the ears and neglected or inadequately treated
middle ear infections. This could impair auditory learning especially in
schools with large class strength and poor acoustics. Most of the learning
in schools is auditory as classrooms may be poorly lit and very little
audiovisual aids may be used. Children with central auditory processing
disorders are often identified after they begin school.

Current Approaches to the Assessment of Hearing in Children

An appropriate audiological assessment of a child can serve the following
purposes.
1. Provide appropriate and timely medical/surgical intervention.
2. Serve a base line.
3. Assist in the selection of appropriate intervention

Behavioral Observation Audiometry (BOA)

This is done by observation of the child’s responses to specified calibrated
stimuli in a structured environment. It is efficient in time, requires
minimum equipment and training. This technique is primarily useful as
an initial hearing screening rather than for any establishment of
thresholds. However, when done carefully by trained observers this
technique can provide valuable initial information about the status of
the child hearing. The audiologist should be skilled in the administration
and interpretation of the child’s responses. In this method, noise makers
 Childhood Communication Disorders 257

and sound field signals (warble tones) are presented. The child’s response
to such stimuli are observed and interpreted.
BOA is used commonly between birth and one year of age. The
contingent responses of the child to different stimuli would be interpreted
with reference to expected responses at that age.
Table 24.7: Development of auditory behavior from birth to sixteen months

Age Response to sound stimuli

Birth-four months Aroused by signals of 90 dB SPL in noisy environment and 50-

70 dB SPL in quiet surroundings.
Three-four months Turns towards the source of sound around 50-60 dB SPL
Four-seven months Turns head directly towards sound between 40-60dB SPL.
Seven-nine months Locates sounds as soft as 30-40 dB SPL
Begins to localize sounds to the side and indirectly below.
Nine-thirteen months Directly locates the sound as low as 25-35 dB SPL to the side and
below
Thirteen-sixteen months Localizes sounds to the side, below and above

It seems that as the child grows older he is able to respond to softer

sounds and also localize sounds on different planes. These auditory
responses of infants that are observed are either reflexive or attentive
behavior. Responses such as head turn, startle, eye blinks, auropalpabral
are classified as reflexive behavior. Attentive behaviors are usually
quieting responses, change in breathing patterns, onset or cessation of
crying, searching, smiling responses.

Techniques to Establish Threshold of Hearing

As the child grows older it is possible to use the behavioral methods
using the principles of operant and classical conditional to establish
thresholds. These include techniques such as visual reinforcement
audiometry (VRA) and tangible reinforcement operant conditioning
audiometry (TROCA). If these procedures are done in free field conditions
using loudspeakers, it is difficult to get ear specific information. Play
audiometry uses classical conditioning techniques, to have the child
respond to the softest sounds heard. Using play audiometry, it is possible
with a cooperative child to obtain a complete audiogram that includes
frequency specific, ear specific information. Routine audiometry with
children will also include information on softest intensities the child
responds to speech stimuli (Speech awareness levels SAL). With children
who have some language it is possible to establish thresholds and speech
recognition scores. Using speech stimuli in testing hearing provides
useful additional information for planning intervention.
258 Selected Topics in Pediatrics for Practitioners

Immittance Evaluation
Assessing of the child’s middle ear function is imperative. Immittance
audiometry provides a simple, non invasive and quick method of
assessing middle ear status. These procedures may be useful especially
for physicians who may not be able to perform an adequate otoscopic
examination or audiologists who are unable to establish audiological
thresholds. Immittance audiometry helps to assess the integrity and
function of the peripheral auditory mechanism. This is achieved by
determining middle ear pressure, tympanic membrane mobility,
eustachian tube function and eliciting the acoustic reflex. The battery of
tests include tympanometry, static compliance, physical volume test
and acoustic reflex measurement. Usually all the four tests should be
interpreted together. Tympanometry is helpful in identifying the type of
pathology in the middle ear such as middle ear effusion, perforation of
tympanic membrane, ossicular discontinuity or stiffness, eustachian tube
dysfunction. The static compliance and physical volume test help in
differential diagnosis of middle ear disorders. The acoustic reflex test is
the determination of the signal threshold level at which the stapedial
muscle contracts. Usually both ipsilateral and bilateral reflexes are
measured. The acoustic reflex threshold is specially a sensitive indicator
of cochlear pathology where the acoustic reflex thresholds are obtained
at sensation levels less than 60dB above the reflex thresholds.

Otoacoustic Emissions
These are low level in audible sounds produced in the cochlea and can
be measured using sensitive equipments. Evoked otoacoustic emissions
can be elicited from normal hearing persons as a release of sound energy
from the ear in response to an external sound. The presence of OAEs is
considered as evidence of normal functioning of the cochlea. These
emissions are rarely recorded in people with hearing loss greater than
30 dB HL. OAEs have an important role in the hearing screening
procedures since they are quick, non-invasive and require no cooperation
from the patients. Increasingly OAEs are being used diagnostically to
differentiate between cochlear and neural pathologies. The identification
of individuals with auditory neuropathy has become easier with the use
of OAEs clinically.

Evoked Response Audiometry (ERA)

These are potentials recorded differentially using electrodes at vertex
and ipsilateral mastoid, with an electrode on the contra lateral ear serving
as ground. These are usually evoked by presenting clicks stimuli audito-
rial. Approximately 2000 clicks are presented and summated by computer
 Childhood Communication Disorders 259

analysis. Click stimuli are used because they have a short rise time that
would evoke synchronous neural bursts. Since clicks are used as stimuli,
the ERA does not provide frequency specific information but rather
information from the basal end of the cochlea (i.e. between 2000 and
4000 Hz). The latency, the amplitude of the waveforms are analyzed. A
robust response is one that is repeatable. An important variable in the
interpretation of ERA, especially in premature infants is the effect of
maturation on the latency and amplitude of the wave forms. By eighteen
months of age the waveforms begin to resemble adult patterns.
The major disadvantage of ERA is that young children need to be
sedated because the test requires minimum movement and takes time.
The results obtained should be interpreted with caution. ERA findings
should not be used as evidence of hearing or of hearing loss unless it
is cross checked with behavioral and immittance audiometry. Today,
ERA is almost routine and recommended by any medical professional
who suspect hearing impairment. It must be well understood that ERA
is not a test of hearing in the perceptual sense and neither can it identify
specific neurological lesion at a specific region. Other auditory evoked
response such as the middle latency response and late auditory evoked
potential, the P300 are also studied especially to identify central lesions.

Auditory Steady State Response (ASSR)

Auditory steady state evoked response is a new tool that enables
frequency-specific hearing assessment in infants and children. The
auditory steady-state evoked response (ASSR) is a brain response elicited
by a continuous or steady-state acoustic stimulus. The brain response to
the steady-state stimulus is also “steady-state”, i.e. it is present over the
duration of the tone used to evoke it. Although the SSR is recorded
using the same montage as for the ABR, the recording and analysis of
the SSR is quite different. The stimulus used to evoke the ASSR is a
modulated tone in the standard audiometric frequency range, 250Hz -
8K Hz. Testing must be carried out while the patient is asleep. The ASSR
is analyzed in the frequency domain using spectral analysis techniques.
The ASSR thresholds are then used to estimate the pure-tone audiogram.
The primary clinical application for ASSR is for detailed frequency-
specific hearing assessment in infants. The estimated audiograms obtai-
ned from ASSR testing provide a basis for determining the most appro-
priate intervention, e.g. recommendation for a hearing aid or conside-
ration for a cochlear implant. One of the primary advantages of ASSR
over conventional ABR and other transient auditory evoked potentials
is the manner in which responses are analyzed. There is no visual
detection of component peaks, nor are peak latencies or amplitudes
measured.
260 Selected Topics in Pediatrics for Practitioners

Intervention
After confirming hearing loss, especially if in early infancy, the process
of selection of a communicative mode must begin. The parents must be
directly involved in this important decision making process. The infor-
mation from initial assessment, qualitative and quantitative develop-
mental information can help in the selection of the appropriate
communication mode. In countries like the USA, parents have sign
language programs, programs advocating total communication, auditory
oral and auditory verbal programs to choose from. In the near future
such options will become available for parents in India too. If the decision
to go into a non-signing program is taken, then no time must be wasted
in fitting a suitable amplification device. Cochlear implants are another
option. With the implementation of the program of free and partially
subsidized hearing aids, securing hearing aids is easier for the
economically weaker sections also. With the fitting of a hearing aid, the
infant should be enrolled in a parent-infant program if available.

Prevention of Hearing Loss

While it is now possible to identify and quantify hearing loss quite early
in life, the challenge is to work towards prevention of hearing loss. The
WHO in 1980, listed infection, neglect and ignorance as main factors
that have caused hearing impairment in India. Any attempt at prevention
has to overcome these three main causes. The infections especially
prenatal causes of hearing impairment have been listed as (TORCHS) T-
Toxoplasmosis, R–Rubella, C-Cytomegalo virus, H Herpes and S-Syphilis.
Among the natal and postnatal causes are measles, mumps, chicken
pox, meningitis, encephalitis, diphtheria and tetanus. Under the causes
related to neglect—are neglect of immunization of pregnant mothers or
post pubertal females for preventable diseases (rubella).
Rh incompatibility, prolonged asphyxia/trauma/infections, neglected
or poorly managed middle ear diseases. There is general ignorance in
the population regarding hereditary deafness and importance of immuni-
zation. As hearing impairment is not a ‘life threatening’ condition medical
professionals are ignorant regarding several causes (especially ototoxic
causes) of hearing impairment. The nature and dosage of drugs used,
the method of administration of the drug, the effective follow up to
control the disease/condition which can be controlled/monitored by
medical professionals may be ignored. This may be due to lack of sensiti-
zation/exposure of medical professionals regarding the ototoxic effects
of medication.
The three levels of prevention are categorized as primary, secondary
and tertiary prevention. With specific reference with hearing impairment,
 Childhood Communication Disorders 261

primary prevention would include programs aimed at preventing hearing

impairment from occurring. This may be through immunization, genetic
education, hearing conservation programs and public/physician
education. The national programs for primary prevention such as the
national measures of immunization, the child survival and safe mother-
hood program, the national nutritional policy are all aimed at prevention
of all disabilities including hearing impairment. Secondary prevention
includes action taken once hearing impairment has developed. Measures
include efforts to either to cure the disease, to stop progress or reverse
the progress. Tertiary prevention includes rehabilitation aimed at
compensating for hearing impairment by providing amplification.

Management of Communication Disorders in Children

There is no doubt that the development of communication is a very
complex process. Effective intervention in individuals with communi-
cative impairments is dependent on careful assessment. Since a child is
constantly maturing, learning and growing, the manifestation of the
communication disorder also changes and evolves over time.
Interventional strategies would also have to be flexible and individualized
to meet the needs of the child. It is very important that the medical and
nonmedical aspects of the disorder should be addressed. The importance
of a medical evaluation and the contribution of nonmedical assessment
such as a language or speech assessment should not be ignored. The
results should be combined while arriving at a diagnosis. Speech
problems are often developmental rather than physiological, and as
such they respond to remedial instruction. Language experiences are
essential for a child’s development. The current philosophy is to keep
the child with a communicative disorder as close as possible to the
mainstream. In order to accomplish this goal, teamwork among the
teacher, speech and language therapist, audiologist, and parents and
other medical professionals is essential. The responsibility of the medical
professional especially pediatrician is to be aware of the early signs of
communication disorders and make appropriate referrals to a speech
pathologist or audiologist and/or others involved in the assessment
process. The role of the pediatrician is also to provide appropriate guida-
nce to parents regarding the possible management and strategies for
many disorders.
Interdisciplinary team work in the best interest of the child. The team
could include the otorhinolaryngologist, neurologist, the psychologist
and among others. Here lies the importance of networking and communi-
cation between medical professionals and a speech pathologist and
audiologist in the management of children with communication
disorders.
262 Selected Topics in Pediatrics for Practitioners

BIBLIOGRAPHY
1. Ansel BM, Landa RM, Luethke LE. Development and Disorders of Speech,
Language, and Hearing. In JA McMillan CD, DeAngelis RD, Feigin and JB
Warshaw (Eds). Oski’s Pediatrics—Principles and Practise (3rd edn). New
York: Lippincott Williams and Wilkins, 1999.
2. Kundu CL. Status of Disability in India-2000. New Delhi: Rehabilitation Council
of India, 2000.
3. Northern JL, Downs MP. Hearing in children (4th edn). Baltimore, Md: Williams
and Wilkins, 1991.
4. Plante E, Beeson PM. Communication and communication Disorders. A Clinical
Introduction. Boston: Allyn and Bacon, 1999.
5. VanRiper C, Erickson RL. Speech correction. An Introduction to Speech
Pathology and Audiology (9th edn). Boston: Allyn and Bacon, 1996.
 25
Child Adoption in India
Chandra Thanikachalam

“Every child has a right to love, and be loved and to grow up in an

atmosphere of love and affection and of moral and material security and
this is possible only if the child is brought up in a family.”

‘Family’ as an institution is accepted worldwide to be the best place for

a child to get its nurture and care for its growth and development.
Therefore placing through adoption is viewed as a superior form of
rehabilitation for an orphaned and abandoned child, compared to
institutional care.

What is Adoption?
Adoption is transfer of rights and responsibilities of a child from its
birth parents to adoptive parents.

Historical Overview
Adoption has been in vogue in India since time immemorial. There were
references of adoption in ancient Indian texts even dating back to 1200
B.C. However, the general impetus for child adoption under the Old
Hindu law practice was for the benefit of the parents to perpetuate
family name and to procure spiritual benefits to the adoptive family.
Hence, only a boy of a nearest relative or of same caste whose parents
were alive, could be adopted by law. Customary practices in those days
generally prohibited adoption of orphans, illegitimate children,
handicapped children and female children.

Hindu Adoption and Maintenance Act-1956

Hindu Adoption and Maintenance Act, which came into force in the
year 1956, has removed to a large extent, the disabilities that were
present in the old law. Under the present act, it is possible to adopt
children of either sex, children of unknown parentage and children who
are differently abled. However, the applicability of the Act is restricted
to Hindus, which includes Buddhists, Jains and Sikhs. Persons belonging
264 Selected Topics in Pediatrics for Practitioners

to other faiths in India do not have an enabling law to legally adopt a

child. Hence they take the other option of becoming a legal guardian of
the child under the Guardian and Wards Act 1890.

Inter Country Adoption

Inter Country Adoptions of Indian minors gained momentum in the
later seventies. From the seventies to early eighties a number of children
were sent abroad by individuals and organisations to be placed in
adoption to foreign nationals. The absence of State sponsored regulatory
measures became a cause of concern, and it motivated a concerned
lawyer, Sri Lakshmikanth Pandey, to seek the intervention of the Supreme
Court of India in this matter. The Supreme Court took serious note of
the situation and after elaborate consultations it delivered its initial
judgement in the year 1984, prescribing norms, ethics and guidelines to
be followed while placing a child in adoption with foreign nationals.
Subsequently a number of clarificatory judgements have been delivered.

Landmark Judgement by the Supreme Court on the Writ Petition

Lakshmikanth Pandey VS Union of India remains till today as established
law on inter-country adoption in India. As a complement to the
judgement, the Government of India brought in Guidelines on Adoption
in 1994. Together, these instruments aim to ensure that the interests and
welfare of surrendered or abandoned minors are protected while placing
them in adoption.

Note
None of the procedural guidelines mentioned in this chapter, other than
the ones specified under The Hindu Adoption and Maintenance Act,
1956, is applicable to direct adoptions where biological parents, or in
their absence, legal guardians, make conscious decision to place a child
in legal adoption with a person of their choice. Hence, hereafter, the
word ‘adoption ‘ wherever it appears, is to be understood as that of an
adoption done by an Adoption Agency and a ‘Child’ means a child who
is surrendered or abandoned by its parents.

Adoption of Indian Minors may Broadly be Classified as

In-country adoption by Indian Nationals living within India. Inter-
country Adoption—by Persons Living Abroad.

Regulations on Adoption Brought in 1984 Onwards

Individuals and unauthorized agencies are prohibited from placing
children in adoption.
 Child Adoption in India 265

Only those agencies, which receive authorization from the concerned

State Governments to do In-Country Adoption may place a child with
Indian Nationals within India.
Only those State Government authorized agencies, which have
obtained special recognition from the Central Adoption Resource Agency
(CARA) to do Inter-Country Adoption, may place a child with persons
living abroad.
Foreign parents are prohibited from directly approaching any person/
agency in India for adoption.
Only a Foreign Adoption Agency enlisted by the Government of
India shall approach a Recognised Indian Agency for adoption – on
behalf of foreign parents.

Order of Priority
Explanation
In order to protect a child’s right to live in the country of its origin and
spare the child from being uprooted from the culture and environment
to which it belongs, the placement agencies have to explore all possibilities
of placing a child in the order of priority as mentioned below.
1. Indian parents living in India
2. Indian parents living abroad
3. At least one parent of Indian origin living abroad
4. Foreign Nationals who are not of Indian origin.

Only a Legally Eligible Child can be Placed in Adoption

Explanation
A child is considered eligible and legally free for adoption on two counts
i.e. when it is surrendered by its parents or declared abandoned by a
competent authority under the Juvenile Justice Act, 2000.

Surrendered Child
Wherever a biological parent or parents wish to surrender their rights
over their child in favour of an agency, authorizing the agency to place
the child in adoption, they execute a ‘Document of Surrender’ in a
stamp paper, with two responsible persons as witnesses. The child will
be considered as legally free for adoption, two months after the execution
of such document.
For a valid surrender the following norms are to be observed:
• In case of legitimate child—both parents have to sign the document
• In case of an unmarried mother—she alone signs
266 Selected Topics in Pediatrics for Practitioners

• Agency which receives the child should counsel the parents:

— to ensure that child surrender is resorted to by the biological
parents as the last option
— that the document of surrender is executed with an informed
consent, out of free will, with no consideration or compensation.

It is also to be noted that

• The biological parents have the right to reclaim the child within 60
days after signing the document.
• Any agreement to surrender the child before its birth is void.

Abandoned Child
Infants and children are voluntarily abandoned by their parents and
families, due to various reasons. They are found everywhere—on the
roadsides, dustbins, hospitals etc, such children must be transferred to
a government—authorized adoption agency immediately.
The adoption agency should follow to these steps after taking custody
of an abandoned child.
• Notify the police
• Notify the Child Welfare Committee (CWC) constituted under the
Juvenile Justice Act 2000.
• Take all steps to trace the parents.
• If not possible, then petition the Child Welfare Committee to issue
a certificate of abandonment.
• After due process of enquiry, if the Child Welfare Committee is
convinced that the child was deliberately abandoned by its family,
it would issue a ‘Certificate of Abandonment’ declaring the child
legally free for adoption.
Two important documents needed for adoption

Home—Study Report
It is a crucial document prepared by the Social Worker of an adoption
placement agency to evaluate a prospective adoptive parents/parent
and must include information on the following issues:
a. Social status and family background
b. Description of home
c. Standard of living
d. Current relationship between husband and wife
e. Relationship of couple and extended members of their families
f. Employment status
g. Health status
 Child Adoption in India 267

h. Accommodation and amenities in the home

i. School facilities for the child
j. Reasons for adoption
k. Attitude of grandparents and other extended members of the family
towards adoption etc.

Child—Study Report
This report would be prepared by the Social Worker of the adoption
agency holding custody of the child. The report would contain
information regarding background of the child including the source its
past and present health history, developmental milestones, behavioural
pattern and etc.

Acts that deal with Child Placement or Adoption

a. The Hindu Adoption and Maintenance Act, 1956.
b. The Guardian and Wards Act of 1890.

The Hindu Adoption and Maintenance Act 1956

People professing Hindu religion that includes Buddhists, Jains and
Sikhs are governed by this Act. The children of either sex, legitimate or
illegitimate, of unknown parentage, abandoned, but brought up as
Hindus are also covered under the definition of this Act.

Salient Features
Who may Adopt?
A Hindu male who is over twenty-one years old and of sound mind
may adopt for himself, if he is single, and with the consent of his wife,
if married.
A female Hindu, who is single in status, i.e. either unmarried,
divorced, or widowed and is over twenty-one years old and is of sound
mind may adopt a child.
A married woman does not have right to adopt but has right to
consent for adoption, when her husband adopts a child. Her right to
adopt can be exercised only, when her husband loses his capacity to
adopt.

Who may be Adopted

Age restriction and marital status will not be a bar in a family or
community where custom or usage permits such adoptions. Any child,
below fifteen years of age, who is a Hindu or brought up a Hindu may
268 Selected Topics in Pediatrics for Practitioners

be adopted. Such a child should not have been already adopted by

somebody or married to somebody.

Who may Give a Child in Adoption

The biological father and in the event of death or disqualification of the
father, then the mother, may give a child in adoption. In the absence of
both, a guardian of the child may place him/her in adoption with the
permission of the Court.

Other Conditions
1. When an adoptive parent wishes to adopt a child of opposite sex,
he/she must be twenty-one years older than that child.
2. An adoptive parent cannot adopt a son, if he/she already has a son,
grandson, or great grandson through his male descendant living or
a daughter if he/she has a biological daughter or son’s daughter
living.
3. Adopted child gets all the rights of a biological child.
4. Such adoption is irrevocable, and an adopted child cannot be placed
on adoption once again.

The Guardian and Wards Act, 1890

Since Indians who are not Hindus, do not have an enabling Law to
adopt a child legally, the next best option available to them is to take
legal Guardianship of the child under the Guardian and Wards Act. But
the child cannot become their own, take their name, or inherit their
property by right. The legal relationship between a Guardian and Ward
would exist until the child completes its 21st year of age.
Foreigners who seek to adopt an Indian child also can file under this
Act, to assume legal Guardianship of the child, after giving an assurance
to the Court, that they would legally adopt the child, as per the Laws
of their country, within two years after the arrival of the child in their
country.

Various Agencies Involved in Adoption and their Functions

Central Adoption Resource Agency (CARA)
In pursuance of the Supreme Court directive CARA was setup by
Government of India. It is functioning as a quasi Government body,
under the Ministry of Social Justice and Empowerment.
Its Functions
• Gives recognition certificates to Authorized Indian Adoption Agencies
to do Inter-country adoption.
 Child Adoption in India 269

• Authorizes reputed Foreign Placement Agencies to co-ordinate in

Inter-country Adoptions.
• Monitors individual cases by issuing No Objection Certificates.
• Formulates Rules and Regulations that is applicable to whole of
India.
• It maintains liaison with Indian Diplomatic missions and furnishes
details of children sent abroad for adoption.
• Acts as clearing house of information on In-Country and Inter-Country
Adoptions.

Authorized Indian Adoption Agencies

These agencies are given special authorization by the concerned State
Government to do adoption placement, strictly within India, and are
subjected to periodic monitoring of the State Government as mentioned
earlier. They must have qualified Social workers on their pay role, counsel
biological parents when they receive the child, take steps to secure
necessary documents to set the child legally free for adoption, and find
suitable prospective adoptive parents after careful evaluation done
through home study report.

Recognized Indian Adoption Agency

An agency which has initially received authorization to do In-Country
adoption may apply to Central Adoption Resource Agency and obtain
a special recognition to do inter-country adoption. Such an agency must
be a reputed one, engaged in other Child Welfare activities apart from
adoption work. It must have other sources of finance and not be solely
dependent on income from adoption services, for its survival. Placing
children within India must be its top priority. When it is unable to find
an Indian parent for a particular child it must register the child with
VCA. If a VCA clearance certificate is issued, then the Agency can take
all steps to locate a suitable family abroad.

Voluntary Co-ordinating Agency (VCA)

It is an association of all licensed adoption agencies in a particular
region and is recognized by the Central Adoption Resource Agency.
Such agencies are created in pursuance of the Supreme Court direction.
The main purpose of this agency is to ensure, that Indian children
get sufficient opportunity to find suitable placements within India. It
maintains a list of eligible prospective adoptive parents, receives
information regarding available children from member agencies, and
tries to match them. Whenever a recognized placement agency is unable
to find an Indian parent for a particular child and wishes to look for a
270 Selected Topics in Pediatrics for Practitioners

foreign parent, it is mandatory for the agency to register the child with
VCA. If VCA is unable to find a suitable Indian family within thirty
days it would issue a clearance certificate stating that it is unable to find
a suitable Indian family. Such a certificate is essential for foreign
placement of the child.

Foreign Sponsoring Agency

These are foreign adoption agencies that have received recognition from
Central Adoption Resource Agency to co-ordinate adoption of Indian
minors in their respective countries.
• Recommends eligible foreign adoptive families, after extensive
evaluation by Professional Social Workers and Psychologists.
• Forwards home study reports and other relevant documents to
recognized Indian placement Agency Routed through CARA.
• Forwards Child study Reports and photographs to the adoptive
parents
• Co-ordinates in matching the child with the family.

Signs following undertakings to the Court

• To protect the interest of the minor until the adoption is legalized in
the receiving Country.
• In the event of disruption in the adoptive family before legalization,
to find alternate family or to escort the child back to India.
• To send follow-up reports to the Court.
Note Foreign Agencies are prohibited
• From Scouting for children in India,
• Establishing contact with biological families,
Unauthorized agencies—for adoptions.

Role of Central Government

• To setup CARA
• To frame approve and amend Rules and Regulations for Inter Country
Adoptions.

Role of the State Governments

• To issue license to do In-Country Adoptions.
• To inspect and supervise the functioning of the adoption agencies.
• To prescribe minimum standards of child care.
• To recommend agencies for Recognition for Inter-Country Adoptions
• To set up adoption cell
 Child Adoption in India 271

Adoption Scrutinizing Agency

Has to be a reputed child welfare agency not involved in child placement
work.
It is appointed by the Court to assist in all matters pertaining
adoptions filed in the Courts.
The scrutiny agency studies documents, verifies facts, makes spot
enquires—to ensure that:
• The child is legally free for adoption.
• Adoptive parents are competent persons
• The laid down- ethics norms and guidelines – being followed
• And that the adoption would be in the best interest of the child.
Calling for the opinion of the Scrutiny Agency is mandatory - for the
Courts in matters of Inter Country Adoptions as per the Supreme Court
Judgments. Number of High Courts have made adoption Scrutiny, a
mandatory procedure even for In-country adoptions.

Two National Bodies—The Indian Council for Child Welfare and Indian
Council For Social Welfare and their branches were recommended by
the Supreme Court of India to be appointed as Adoption Scrutinizing
Agencies if found eligible.

Procedure for In-country Adoption

Prospective Indian adoptive parents who wish to adopt/take
guardianship of a child shall register either with an authorized placement
agency or The Voluntary Coordinating Agency of the region. A
professionally qualified social worker of the agency shall interview the
couple, examine the family and prepare a detailed Home Study Report.
Once they are found to be competent persons to adopt, they will be
matched with a child, as per the requirement of the parents. Generally
parents are discouraged to go around shopping for a child, and they
would be shown only one child at a time.
Finally when the parents decide to adopt, they will be asked to sign
a foster-care agreement to take custody of the child. If after six months,
the integration of the child with the family is found successful, they will
be permitted to petition in the competent court, either under the HAMA
or the GWA, as the case may be.
They will be allowed to verify the child’s medical records, and to
take a pediatrician of their choice to examine the child. They will be
permitted to subject the child for further medical investigation if
necessary. The cost of such investigation will be borne by the parents.
272 Selected Topics in Pediatrics for Practitioners

Procedure for Inter-Country Adoption

Foreign Nationals or persons living abroad, who is desirous of adopting
an Indian minor shall first make an application to Enlisted Foreign
Agency who has the closest geographical proximity to their place of
residence.
The Social Worker of the Agency would do an in-depth study of the
family and prepare a Home Study Report. Once certified to be eligible,
their application will be forwarded, with their specific requirement,
through proper channel (i.e. through the Indian embassy of that country
and CARA) to an Indian Recognized Placement Agency.
The Indian Recognized placement Agency, will match a child, that
meets with the requirement of the adopter, with reference, to age, sex,
normal/special needs and, etc. The Agency would send in the photograph
and the Child Study Report with detailed medical history and social
background.
The Foreign Agency in turn would forward the same to the prospective
Adoptive Parents and get their letter of consent to adopt the child. At
this juncture, the prospective adoptive parents may even be permitted
to meet with the child if they under take to travel and come to India.
After obtaining No-objection certificate from CARA the Indian
placement agency will make a petition in the competent Court in India
as Power of attorny to the prospective adoptive parents.
The petition would be to request the Court to appoint the foreigners
as guardians of the child, under the Guardian and Wards Act, 1890 with
a permission to remove the child to the Country of resident of the
parents for future adoption.
The Court would send the notice to the Adoption Scrutinizing Agency
referring the matter and calling for report. After obtaining the Scrutiny
Report, if the petitioners are found competent persons, Orders would be
issued appointing the foreigners as guardians for the minor with
permission to remove the child out of the country with the following
conditions:
• that they would legally adopt the child as per the laws of the country
where they reside.
• that they would comply with the orders to send follow up reports.
After obtaining Court orders the Indian placement Agency would
make necessary steps to obtain passport and other travel documents
and escort the child to the foreign adoptive parents. Until the child is
legally adopted as per the laws of the receiving country, and the
citizenship is changed, the child will be under the control of the Indian
Embassy and the Indian Court.
 26
Pediatricians and Adoption
Ananthalakshmi

A frequently raised question by pediatricians is “How liable am I, if a

couple of months after recommending an infant for adoption a health
condition surfaces?”
This anxiety flows from a misconception that recommendation of an
adoptive child for adoption to a Prospective Adoptive Parent (PAP)
reduces the pediatrician to a guarantor. The fear of the unknown restrains
and inhibits the pediatrician from assuring a positive outlook towards
the adoption scenario.
However, the pediatrician must be reminded that he/she has a
medico-social responsibility towards promoting adoption. To discharge
this responsibility more meaningfully and with greater understanding,
the pediatricians have to be first made aware of the adoption process
and be sensitized to the background of the adoptive child as also the
needs of the Prospective Adoptive Parent.
The adoptive infant is an unknown identity, in the sense that little
is known about the birth history of the child. If the child happens to be
an abandoned baby, the date of birth as also the parentage is unknown.
A research undertaken a couple of years back for database creation in
adoption, revealed that 74 per cent of children in the adoption stream
were born to unwed mothers, a majority of whom were teenagers and
their identity kept a closely guarded secret for obvious reasons. Infants
who enter the adoption stream whether surrendered or abandoned are
babies who are basically unwanted. Being unwanted they are subject to
a great degree of foetal violence. Consequently when they are born they
are underweight, undernourished, marasmic and have delayed mild
stones.
Besides the babies are relinquished by the mothers within days or a
few weeks of their birth. The placement agency, which is a voluntary
child care organization, licensed to place children in adoption, to whom
the baby is surrendered, takes over the care, food and health needs of
the child. The child to be legally free for adoption should have completed
two months of age. These two months are really a period granted for
the mother to reclaim the child.
274 Selected Topics in Pediatrics for Practitioners

During this waiting period and till such time a suitable adoptive
parent is found for the baby, the infant is removed from the mother and
deprived of the mother’s care and feeding. The baby is fed on substitute
milk and is under institutional care.
Maternal deprivation has a long term emotional impact—the infants
suffer from a “separation anxiety”. If kept under institutional care for
a long time they are likely to suffer from a “failure to thrive syndrome”.
With poor weight and given feeding patterns they lack touch and stimuli.
The infants who remain in the institute for a couple of years develop
“institutional child syndrome”. One of the features of institutional
syndrome is failure to treat on account of multiple mothering which
means that care given change every eight hours and the infant does not
feel the same arm and warmth. As a result, the children suffer from
delayed milestones, development delays, poor motor development
coordination poor eye contact etc. these can be overcome to a large
extent if infants are placed in loving caring families.
A pediatrician is centric to the process of adoption. He/she is required
to give parenting advice and emotional support to the Prospective
Adoptive Parent.
Two case studies of almost similar nature throw light on the crucial
role of a pediatrician in promoting adoption. Child X and Child Y
weighed 1.3 kg and 2 kg at the time of birth. Their anthropometric
measurements were within prescribed limits. The health study of these
infants revealed that child X was malnourished and Child Y had mild
delayed milestones. Child X was placed in adoption but Child Y was
rejected. The encouragement, assurance and support given by the
pediatrician in the first case was instrument to the placement. Infants
who have undergone fistulectomy, HIV +ve turned –ve have all been
placed with positive guidance of the pediatrician.
Consider the following conditions on account of which children have
not been accepted for adoption and therefore given clearance for
intercountry adoption under the category of “special needs” children.
• Hypothyroidism
• HBsAg positive
• CMV positive
• Acute gastroenteritis with hypernatremia
• Thyroglossal fistula
• Congenital ichthyosis, of the skin, idiopathic genu valgum
• Infantile hemiparesis, delayed language, moderate MR
• Birth asphyxia—mild MR
• Pyloric stenosis
• Ventricular septal defect, mild pulmonary hypertension with left to
right shunt
 Pediatricians and Adoption 275

• Congenital heart disease, severe pulmonary hypertension

• Septicemia and septic arthritis
• Malformed left external ear with rudimentary external ear canal
• Perineal abscess in the rectum
• Coronal hypospadias
• Bilateral idiopathic genu-varum
• Thalassemia
• Myoclonic jerks, tuberous sclerosis, multiple angiofibromata on the
face
• Anterior staphyloma in the right eye (secondary to keratomalacia)
• Enlargement of the left kidney
• Microcephaly
• Acute gastroenteritis with renal tubular acidosis
• Left peritracheal mass lesion
• Acute diarrheal disease with UTI, renal tubular acidosis, laryngo-
malacia
• Borderline delayed milestone, has features of lipid storage disorder
• Mass lesion seen in the left parotid gland tonsillo pharyngitis
• Wheezy bronchitis
• Diarrheal episodes
• Phimosis
• Febrile seizures
• Habit disorder breath holding spell
• Stridor-congenital
• Hemangioma
A perusal of the list makes it clear that not all the health conditions
notified are beyond treatment and often the easy way out is to tell the
Adoptive Parent “you are anyway going to adopt, you might as well
take a healthy child”. No statement can be more damaging and insulting
to the adoptive child than this.
Yet families in the west come forward to adopt such children. If this
can be so why not our adoptive parents do the same? Granted it is an
emotional issue and adoption is a matter of choice. But it is here that
the pediatrician has a vital role to sensitize the Prospective Adoptive
Parent to the needs of the child and the consolation that the Prospective
Adoptive Parent may derive in caring for such children. It certainly is
glamorous to grow up in the west. However, in the final analysis the
ethnic card could cause a great deal of emotional disturbance. It is an
accepted fact that “ the child develops best in his or her own cultural
and social milieu” and placement of a child through adoption in an
indigenous setting would be ideal for his or her growth. In this, the
pediatrician has a crucial role to play. In the process of adoption the
pediatrician is not only a pediatrician but needs to be a pediatric-adoptive
parent consultant.
 28
Pediatrician in the Year 2033
RK Agarwal

“The good physician knows his patients through and through, and his
knowledge is bought dearly. Time, sympathy and understanding must
be lavishly dispensed, but the reward is to be found is that, personal
bond which forms the greatest satisfaction of the practice of medicine.
One of the essential qualities of the clinician is interest in humanity, for
the secret of the care of the patient is in caring for the patient.”
Dr Francis weld Pedbody 1927

This write up is intended to understand our past in a better way. It

is the knowledge and influence of the past, which lets one of us
understand the realities of present in proper perspective. If one foresees
correctly, is a concern for all of us. In the past and to some extent in our
later times, there was a personal relationship with the patients and their
parents. They respected us as individuals, well qualified and well trained
as their health keepers. There was a relationship built on trust. This
mutual and familial relationship was more highly valued than money.
The patient would pay money but still bend down to touch the feet and
would say with folded hands thanks to show his gratefulness. A word
noble was attached to this profession. A doctor’s presence in any social
gathering was always conspicuous and he was always looked upon
with great respect. This relationship is fast changing even while I am
writing this the changes are being driven by globalization, economic
priorities and mechanical technology with gadgets and we are heading
slowly into a ditch.
The world is facing many changes. The attitudes, preferences and
priorities of majority of people are now different. A vast majority of
human race is chasing its dreams and aspirations at feverish pitch and
in the process forgetting and ignoring basic emotional and spiritual
needs. There is a perceptible imbalance in the total human environment.
Somewhere, the human race is having a feeling of suffocation. The inner
peace and harmony appears to be illusive like never before.
Even these days we are seeing a big change in public perception of
medicine. The doctors are now termed as health care providers and the
patients like to be called consumers. Advertising and professional
322 Selected Topics in Pediatrics for Practitioners

promotion techniques have changed the image of a pediatrician. Parents

are fascinated with technology and have begun trusting in it more than
the clinical skills of a child specialist. This decrease in trust is difficult
for me and like-minded colleagues to accept. We have always considered
ourselves as advocates of child welfare. MBBS truly spells “Moral
Betterment and Better Services” for me.
We have much less intense role in taking clinical and direct care of
patients at present. Technicians and nursing staff probably deliver most
medical care. That is the natural outcome of advanced technology and
machines. I find even today the doctors are accepting the superiority of
an instrument over interpreter of its finding and concluder of diagnosis.
Because we are not devoid of these, we don’t even realize the classic role
of a critical thinker and diagnostician which has been snatched away by
technological advances such analysis and treatment programs, robotic
imaging scanners and automated laboratories. Genetic engineering would
probably have eliminated many physical defects and diseases, which
one could only ameliorate. These technologies, born in all lifetime are
undeniable scientific wonders.
With all these so called ‘hi fi’ advancements, the healing physician
in us is bound to diminish. In the company of gadgets, the future
generations pediatrician would probably have been reduced to a spiritless
instrument. The feel in his voice, his touch, his comforting look is what
he may be lacking. The soothing voice of the physician saying, I dream
your dreams, I perceive your pain, I share your mortality, therefore, I
understand your suffering that is what we have always been about.
Thus the domain of the physician is not restricted to the physical
being as is technology. The biggest mockery is that even the super
computer does not think. We are allowed beyond that temporary temple.
We have access to spirit.
As a healer of the body, we have been superbly trained. As a future
generation pediatrician and as a caretaker of this ‘Hippocratic spirit’,
you must preserve a personal relationship with the patients and their
families. To touch a child with healing hands may be our job but to
instill hope is to continue the heritage and nobility of our age old
profession. We are counting on the future pediatricians.
The scenario is of a sick and suffering child who is also scared because
he does not understand what is ailing him, being brought in my chamber
by anxious parent but by the time they leave, the child is smiling (though
still having pain and fever) and the parent is reassured of humane and
holistic (wholistic) care by a caring pediatrician. It is ardently hoped that
thirty years hence the scenario remains the same with added benefit of
more accurate and speedy diagnosis and more scientific treatment
centered on evidence based medicine. This is possible only if the future
 Pediatrician in the Year 2033 323

generation of pediatricians possess the sagacity of a proper amalgamation

of and balance between technology and humane values. I am confident
that they may have this sagacity.

BIBLIOGRAPHY
1. RK Agarwal. Food for thought for the future. In RK Agarwal (Ed): Pediatrician;
News letter, Udaipur Chapter IAP 2003;1-2.
 Annexure 1
Normal Laboratory Values
HPS Sachdev, Piyush Gupta

The Normal Range

Results of a laboratory test can be interpreted in terms of being normal or abnormal,
and negative or positive only on the basis of already known normal of reference
values. Normal values refer to those measurements which are usually central and
around which most of the values lie in the healthy individuals.
Almost all normal laboratory values are represented and expressed in a reference
range and rarely in terms of a single measurement. For example, a large group of
healthy children in the age group of 6-12 years may have an average hemoglobin
of 14.0 g/dl with individual values ranging from11.5 to 15.5 g/dl. In this case, the
normal hemoglobin values in 6-12 years old are said to range between 11.5-15.5 g/
dl and not simply 14.0 g/dl. The normal or reference range is an integral part of all
laboratory values because of considerable magnitude of interindividual variability
in the normal population. Variations in normal subjects occur due to a host of
reasons that may include biological, genetic, environmental in creating a rather wide
range of values that may be referred to for classifying an individual as having a
normal or abnormal laboratory test.
The central values are measured in terms of mean, median and mode. Fortunately,
these three measures generally coincide in most of the laboratory measurements in
healthy individuals. The normal deviation around the mean is termed as standard
deviation. In a typical Gaussian (bell-shaped) distribution curve. 95 percent of the
normal values lie between ± 2 SD around the mean. However, certain laboratory
values in normal individuals do not follow the Gaussian curve, making it difficult
to assume all values within mean ± 2SD as being normal. In such situation, the
normal values are expressed in terms of a range covering 95 percent of values from
a set of values found in a healthy population, excluding 2.5 percent each of the
lowermost and uppermost values.
Most of the laboratory tests do not have any absolute or magic cut-off point for
labeling their results as being normal and abnormal. For example, if normal range
of values of blood urea nitrogen is 5-18 mg/dl, in children, then 17 mg/dl carries
an importance equivalent to a value of 19 mg/dl. Both these values are then termed
as borderline. Such borderline values can be present in healthy as well as sick
subjects and should be interpreted cautiously. Biological lab values may have small
variations between individual labs depending on their methodology. Hence it is
useful to compare the estimated value with norms given along side in the report.

PREDICTIVITY OF THE TEST

Most of the time results of a laboratory test are not intended to be diagnostic. To
make the diagnosis, one may have to carry out multiple tests or other investigations
326 Selected Topics in Pediatrics for Practitioners

such as radiography, microbiological isolation and antigen or antibody detection

apart from proper evaluation of the clinical presentation.
Laboratory tests, based on a single criteria may only suggest that a person may
or may not be having the disease. Validity of the test is estimated by its is estimated
by its sensitivity and specificity. Sensitivity is defined as the ability of a test to
correctly identify those who have the disease. An ideal laboratory test should be
both 100 percent sensitive and specific. Practically, this is never the case. The results
of a laboratory test are compared with that of a diagnostic test in order to find the
validity.

For example
A = Laboratory test done to find out the probability of a condition (results in
abnormal or normal)
B = Diagnostic test done in the same subjects to find out the presence of disease
(disease present to absent)
The results of A and B are compared as follows:
A B Total
Disease present Disease absent
Abnormal (positive) a b A+b
Normal (negative) c d C+d
Total a+c b+d a+b+c+d

a = number of those who had both positive laboratory and diagnostic tests (true-
positives).
b = number of those who had a positive laboratory test, but were not undiseased
(false-positive).
c = number of those who had a negative laboratory test, but found diseased
(false-negative).
d = number of those who had both negative laboratory and diagnostic test (true-
negatives).
a
i. Sensitivity = × 100
a+c
d
ii. Specificiy = × 100
b+d
b
iii. Percentage of false-positives = × 100
b+d
c × 100
iv. Percentage of false-negatives =
a+c
In addition of validation of measuring specificity and sensitivity, the diagnostic
power of the test can also be calculated by the predictive value of the test. Predictive
value is dependent on: (i) specificity, (ii) sensitivity, and (iii), the prevalence of the
disease. The higher the prevalence, the more likely it is that a positive among all
those who have positive test results.
a
v. Predictive value of a positive test = × 100
a+b
 Annexure 1: Normal Laboratory Values 327

d
vi. Predictive value of a negative test = × 100
c+d
The Predictive value of a positive test indicates the probability of a person with
a positive diagnostic test as well. If the prevalence of a disease is low, even a highly
valid test will yield a low predictive value. A disease with a high prevalence is likely
to result in a more accurate predictive value of positive laboratory test.

COMMON ABBREVIATIONS
Most of the commonly used units are written in an abbreviated form. A list of such
units is given below in Table 1.
Table 1: Abbreviations for common units.
Units Unit names Abbreviations
Time Year, month, week, day, Yr, mo, wk, hr, min, s
hour, minute, second
Weight gram g
Length meter m
Capacity liter L
Pressure millimeter of mercury mm Hg
Enzyme activity International unit I
Volume cubic millimeter mm3
Osmolality mole mol
Equivalent weight milliequivalent mEq

Various prefixes are used along with the units of length, capacity and mass. A
list is given in Table 2.
Table 2: Prefixes used for decimal factors
Prefixs Symbols Factors
Mega M 106
Kilo k 103
deci d 10-1
centi c 10-2
milli m 10-3
micro μ 10-6
nano n 10-9
pico p 10-12
femto f 10-15

NORMAL HEMATOLOGICAL VALUES

Blood volume
males 52-83 mL/kg
females 50-75 mL/kg
Plasma volume
males 25-43 mL/kg
females 28-45 mL/kg
Total RBC Count
cord blood 3.9-5.5 × 1012 Cells/L
328 Selected Topics in Pediatrics for Practitioners

1-3d 4.0-6.6 × 1012 Cells/L

1 wk 3.9-6.3 × 1012 Cells/L
2 wk 3.6-6.2 × 1012 Cells/L
1 mo 3.0-5.4 × 1012 Cells/L
2 mo 2.7-4.9 × 1012 Cells/L
3-6 mo 3.1-4.5 × 1012 Cells/L
0.5-2 yr 3.7-5.3 × 1012 Cells/L
2-6 yr 3.9-5.3 × 1012 Cells/L
6-12 yr 4.0-5.2 × 1012 Cells/L
Total WBC count
birth 9.0-30.0 × 109 Cells/L
24 h 9.4-34.0 × 109 Cells/L
1 mo 5.0-19.5 × 109 Cells/L
1-3 yr 6.0-17.5 × 109 Cells/L
4-7 yr 5.5-15.5 × 109 Cells/L
8-13 yr 4.5-13.5 × 109 Cells/L
Differential leukocyte count
Mean percentage

Neutrophils Lymphocytes Eosinophils Monocytes

Cord blood 61 31 2 6
2 wk 40 48 3 9
3 mo 30 63 2 5
6 mo-6 yr 45 48 2 5
7-12 yr 55 38 2 7

Total neutrophil count

bands 15-400 × 106 Cells/L
segmented 3000-5800 × 106 Cells/L
Total lympocyte count 150-3000 × 106 Cells/L
Total monocyte count 285-500 × 106 Cells/L
Total eosinophil count 50-250 × 106 Cells/L
Total basophil count 15-50 × 106 Cells/L
Total myelocyte count Nil
Reticulocyte count
1-7 d 0.4-6% of erythrocytes
Children 0.5-1.5% of erythrocytes
Platelet count
<7d 84-478 × 109 Cells/L
>7d 150-400 × 109 Cells/L
Hematocrit
1-3 d 45-75%
2 mo 28-42%
6-12 yr 35-45%
adolescent male 37-49%
adolescent female 36-46%
Hemoglobin
1-3 d 14.5-22.5 g/dL
2 mo 9.0-14.0 g/dL
6-12 yr 11.5-15.5 g/dL
adolescent male 13.0-16.0 g/dL
adolescent female 12.0-16.0 g/dL
 Annexure 1: Normal Laboratory Values 329

Hemoglobin A
> 95% of total hemoglobin
Hemoglobin A2
1.5-3.5% of total hemoglobin
Fetal hemoglobin
newborn 60-90% of total hemoglobin
3 months 2-59% of total hemoglobin
6 months 2-9% of total hemoglobin
> 1 year <2% of total hemoglobin
Glycohemoglobin
Total 4-16 yr 6-10% of total hemoglobin
1-5 yr 2.1-7.7% of total hemoglobin
5-16 yr 3-6.2% of total hemoglobin
Methemoglobin
0.06-0.24 g/dL
Red cell volume
Male 20-36 mL/Kg
Female 19-31 mL/Kg
Mean corpuscular hemoglobin (MCH)
0-3 d 31-37 pg
1 mo 28-40 pg
3 mo 25-35 pg
1 yr 23-31 pg
2-6 yr 24-30 pg
6-12 yr 25-33 pg
Mean corpuscular hemoglobin
Concentration (MCHC)
All ages 30-37
Mean corpuscular volume (MCV)
0-3 d 95-121 fL
6 mo –2 yr 70-86 fL
6-12 yr 77-95 fL
adolescent 80-100 fL
Erythrocyte sedimentation rate (ESR)
Westergren 0-10 mm/hr
Wintrobe 0-13 mm/hr

MEASURES OF COAGULATION
Clotting time
5-8 min in glass tube
Bleeding time
2-7 min normal
7-11 min borderline
Partial thromboplastin time (PTT)
nonactivated 60-85 s
activated (APTT) 25-35 s
infant < 90 s
Thrombin time (TT)
Control time +2 s (normal control 9-13 s)
Fibrinogen
newborn 1.25-3.00 g/L
children 2.00-4.00 g/L
330 Selected Topics in Pediatrics for Practitioners

Fibrin degradation product (FDP)

< 10 mg/L
Coagulation factors
Factor I (as above see fibrinogem)
Factor II 60-150% of normal or AU
Factor V 60-150% of normal or AU
Factor VII 65-135% of normal or AU
Factor VIII 60-145% of normal or AU
Factor VIII 50-200% of normal or AU
antigen
Factor IX 60-140% of normal or AU
Factor X 60-130% of normal or AU
Factor XI 65-135% of normal or AU
Factor XII 65-150% of normal or AU

SERUM BIOCHEMISTRY
Serum proteins (g/dL)
Total Albumin α 1 glo- α 2 glo- β glo- γ glo-
bulin bulin bulin bulin
Preterm 4.3-7.6 3.0-4.2 0.1-0.5 0.3-0.7 0.3-1.2 0.3-1.4
New born 4.6-7.4 3.6-5.4 0.1-0.3 0.3-0.5 0.2-0.6 0.2-1.0
Infant 6.1-7.9 4.0-5.0 0.2-0.4 0.5-0.8 0.5-0.8 0.3-1.2
Thereafter 6.4-8.2 3.5-5.0 0.2-0.3 0.4-1.0 0.5-1.1 0.7-1.2

Plasma albumin
preterm 1.8-3.0 g/dL
term newborn 2.5-3.4 g/dL
< 5 yr 3.9-5.0 g/dL
5-19 yr 4.0-5.3 g/dL
Serum bilirubin (mg.dL)
Term Preterm
Cord blood < 2.0 < 2.0
0-1 d < 6.0 < 8.0
1-2 d < 8.0 < 12.0
2-7 d < 12.0 < 16.0
>7d 0.2-1.0 < 2.0
Conjugated bilirubin 0-0.2 mg/dL
Serum Urea
cord blood 21-40 mg/dL
preterm 3-25 mg/dL
term newborn 3-12 mg/dL
< 1 year 5-18 mg/dL
< 1 year 7-18 mg/dL
Serum Creatinine
cord blood 0.6-1.2 mg/dL
neonate 0.3-1.0 mg/dL
< 1 year 0.2-0.4 mg/dL
2-12 year 0.3-0.7 mg/dL
adolescent 0.5-1.0 mg/dL
 Annexure 1: Normal Laboratory Values 331

Serum Glucose
cord blood 45-96 mg/dL
newborn 40-90 mg/dL
children 60-100 mg/dL
Glucose tolerance test (GTT), oral
glucose administered in a dose of 1.75 g/kg, max: 75 g
Normal Diabetic
fasting 70-105 > 115 mg/dL
60 min 120-170 > 200 mg/dL
90 min 100-140 > 200 mg/dL
120 min 70-120 > 140 mg/dL
Serum Galactose
newborn 0-20 mg/dL
Serum Cholesterol
1-3 year 45-182 mg/dL
4-6 year 109-189 mg/dL
6-9 year 122-209 mg/dL
10-14 year 124-217 mg/dL
Serum Ammonia
newborn 64-107 µmol/L
0-2 wk 56-92 µmol/L
> 1 mo 21-50 µmol/L
thereafter 11-32 µmol/L
Serum Ammonia
newborn 64-107 mg/dL
infant 100-275 mg/dL
child 180-295 mg/dL
Serum Phospholipids
newborn 75-170 mg/dL
infant 100-275 mg/dL
child 180-295 mg/dL
Myoglobin
6-85 mg/mL
Serum Triglycerides (mg/dL)
Male Females
cord blood 10-98 10-98
0-5 year 30-86 32-99
6-11 year 31-108 35-114
12-15 year 36-138 41-138

METALS AND BINDING PROTEINS

Iron
newborn 100-250 µg/dL
infant 40-100 µg/dL
child 50-120 µg/dL
older age males 50-160 µg/dL
females 40-150 µg/dL
Iron Binding Capacity (TIBC)
< 1 year 100-400 µg/dL
> 1 year 250-400 µg/dL
332 Selected Topics in Pediatrics for Practitioners

Serum Transferrin
1-3 year 218-347 mg/dL
4-9 year 208-378 mg/dL
10-19 year 224-444 mg/dL
Serum Ferritin
newborn 25-200 ng/mL
1 month 200-600 ng/mL
2-5 month 50-200 ng/mL
6 month, 15 year 7-14 ng/mL
Serum Copper
0-5 month 9-46 µg/L
1-9 year 80-150 µg/dL
10-14 year 80-121 µg/dL
15-19 year 64-160 µg/L
Serum Ceruloplasmin
0-5 d 5-26 mg/dL
1-19 year 20-46 mg/dL
Serum Magnesium
0-6 d 1.2-2.6 mg/dL
7 d-2 year 1.6-2.6 mg/dL
2-14 year 1.5-2.3 mg/dL
Blood Lead
children < 10 µg/dL
adults < 40 µg/dL
toxic ≥ 100 µg/dL
Serum Zinc
64-118 µg/dL

SERUM ENZYME LEVELS

Serum Amylase
35-127 U/L
Serum Aldolase
10 mo-2 yr 3.4-11.8 U/L
2 yr-16 yr 1.2-8.8 U/L
Serum Alkaline Phosphatase
1-9 year 145-200 U/L
10-11 year 130-560 U/L
Male Female
12-13 year 200-495 U/L 150-420 U/L
14-15 year 130-525 U/L 70-230 U/L
16-19 year 65-260 U/L 50-130 U/L
Serum Aspartate Aminotransferase (AST, SGOT)
0-5 d 35-140 U/L
1-9 yr 1-55 U/L
10-19 yr 5-45 U/L
Serum Alanine Aaminotransferase (ALT, SGPT)
0-5 d 6-50 U/L
1-19 yr 5-45 U/L
Creatine Kinase
Cord 70-380 U/L
Newborn 87-1200 U/L
Adult 5-130 U/L
 Annexure 1: Normal Laboratory Values 333

Serum Creatine Kinase Isoenzymes

CKMB CKBB
Cord 0.3-3.1 0.3-10.5%
0-24 hr 1.7-7.9% 3.6-13.4%
72-100 hr 1.4-5.9% 5.1-13.3%
Older 0-2% 0
Blood Glucose 6 phosphate Dehydrogenase (G6PD)
Adult 3.4-8.0 U/g Hemoglobin or
1.16-2.72 U/mL RBC

The values are 50 percent higher in newborns

Serum Lactate Dehydrogenase (LDH)
<1 yr 170-580 U/L
1-9 yr 150-500 U/L
10-19 yr 120-330 U/L
Serum-α1antitrypsin
0-5 d 143-440 mg/dL
1-9 yr 147-245 mg/dL
9-19 yr 152-317 mg/dL

Normal Acid-Base Status And Electrolytes

Oxygen Partial Pressure (PaO2) (Arterial)
birth 8-24 mm Hg
5-10 min 33-75 mm Hg
30 min 31-85 mm Hg
>1 hr 55-80 mm Hg
1d 54-95 mm Hg
thereafter 83-108 mm Hg
Oxygen Saturation (arterial SaO2)
newborn 85-90%
thereafter 95-99%
Carbon Dioxide Partial Pressure (PaCO2)(Arterial)
<1 yr 27-40 mm Hg
thereafter 32-48 mm Hg
Serum bicarbonate (HCO3)
arterial 21-28 mmol/L
venous 22-29 mmol/L
Base Excess
newborn -10 to –2 mmol/L
infant -7 to –1 mmol/L
child -4 to +2 mmol/L
older -3 to +3 mmol/L
pH
birth 7.1-7.36
30 min 7.2-7.38
1d 7.3-7.45
older children 7.35-7.45
Serum Osmolality
275-295 mOsm/kg H2O
334 Selected Topics in Pediatrics for Practitioners

Serum Sodium
newborn 134-146 mmol/L
<1 yr 139-146 mmol/L
children 138-145 mmol/L
Serum Potassium
<2 yr 3.0-6.0 mmol/L
2-12 yr 3.0-6.0 mmol/L
>12 yr 3.5-5.0 mmol/L
Serum Calcium
newborn 9.0-12.0 mg/dL
child 8.8-10.8 mg/dL
Serum Chloride
newborn 96-110 mmol/L
child 98-106 mmol/L
Inorganic Phosphorus
newborn 4.8-8.2 mg/dL
1-3 yr 3.8-6.5 mg/dL
4-11 yr 3.7-5.6 mg/dL
12-15 yr 2.9-5.4 mg/dL
Anion gap
7.16 mmol/L

HORMONE LEVELS IN SERUM AND URINE

Plasma Adrenocorticotrophic Hormone (ACTH)
Cord blood 130-160 pg/mL
1-7 d postnatal 100-140 pg/mL
adult
morning 25-100 pg/mL
evening <50 pg/mL
Plasma serum Aldosterone
(levels on normal sodium intake In supine position)
neonate 5-18 ng/dL
infants 5-90 ng/dL
1-2 yr 7-54 ng/dL
2-10 yr 3-35 ng/dL
10-15 yr 2-22 ng/dL
Values are elevated, when measured in upright subjects.
Urinary Aldosterone
Newborn 0.5-5 μg/24 hr
4-10 yr 1-8 μg/24 hr
older 3-19 μg/24 hr
Plasma Antidiuretic hormone (ADH) varies with Plasma osmolarity
Plasma Osmolarity Plasma ADH
270-280 mOsm/kg <1.5 pg/mL
280-285 mOsm/kg <2.5 pg/mL
285-290 mOsm/kg 1-5 pg/mL
290-295 mOsm/kg 2-7 pg/mL
295-300 mOsm/kg 4-12 pg/mL
 Annexure 1: Normal Laboratory Values 335

Plasma Cortisol
newborn 1-24 μg/dL
adults
morning 8 a.m 5-23 μg/dL
evening 4 p.m 3-15 μg/dL
night 8 p.m less than 50 percent of morning level
Free Urinary Cortisol
child 2-27 μg/24 hr
adolescent 5-55 μg/24 hr
Plasma Growth Hormone
neonate 5-27 ng/mL
infant 2-10 ng/mL
child <0.7-6 ng/mL
Plasma Insulin (12 hr fasting)
newborn 3-20 μU/mL
thereafter 7-24 μU/mL
Serum Prolactin
male 3-18 ng/mL
female 3-24 ng/mL
Serum Parathyroid Hormone (PTH)
C-terminal 51-217 pg/mL
intact 1-43 pg/mL
intact N terminal 14-21 pg/mL
Plasma Renin Activity
0-3 yr <16.6 ng/mL/hr
3-6 yr <6.7 ng/mL/hr
6-9 yr <4.4 ng/mL/hr
9-12 yr <5.9 ng/mL/hr
12-15 yr <4.2 ng/mL/hr
Urinary 17 OHCS (hydroxycorticosteriod)
0-1 yr 0.5-1.0 mg/24 hr
child 1.0-5.6 mg/24 hr
adults
Male 3.0-10.0 mg/24 hr
Female 2.0-8.0 mg/24 hr
Urinary 5HIAA (hydroxyindoleascetic acid)
2-8 mg/24 hr
Serum 17OHP (hydroxyprogesterone)
newborn
preterm 26-568 ng/dL
term 7-77 ng/dL
infant children
male 40-200 ng/dL
female 13-106 ng/dL
Urinary 17KS (Ketosteriods)
14 d-2 yr <1 mg/24 hr
2-6 yr <2 mg/24 hr
6-10 yr 1-4 mg/24 hr
10-12 yr 1-6 mg/24 hr
12-14 yr 3-10 mg/24 hr
14-16 yr 5-12 mg/24 hr
336 Selected Topics in Pediatrics for Practitioners

Urinary 17KGS (ketogenic steriods)

0-1 yr <1.0 mg/24 hr
1-10 yr <5 mg/24 hr
11-14 yr <12mg/24 hr
Total Tri-iodothyronine (T3)
cord blood 30-70 ng/dL
newborn 75-260 ng/dL
1-5 yr 100-260 ng/dL
5-10 yr 90-240 ng/dL
10-15 yr 80-210 ng/dL
Total Thyroxine (T4)
Newborn 8.2-19.9 μg/dL
Infant 6-15.0 μg/dL
1-3 yr 6.8-13.5 μg/dL
3-10 yr 5.5-12.8 μg/dL
Thyroid Stimulating hormone (TSH)
Cord blood 3-12 μU/mL
Newborn 3-18 μU/mL
Thereafter 2-10 μU/mL

NORMAL URINARY VALUES

Volume (24 hours)
Neonate 50-300 mL
Infant 350-500 mL
Child 500-1000 mL
Adolescents 700-1400 mL
Specific Gravity
24 hr urine 1.05-1.025
after fluid >1.025
restriction for 12 hrs
Osmolality
50-1400 mOsm/kg water
after fluid
restriction >850 mOsm/kg water for 12 hrs
pH
neonatal period 5-7
children 4.5-8 (mean 6.0)
Cell count
Red blood cells 0-2/hpf
White blood cells 0-5/hpf
Epithelial cells few
Bacteria 0-20 organisms in centrifuged specimen
Casts
Hyline cast 0-1/hpf
RBC, WBC absent
Epithelial casts
Proteins
Total (24 hours) 50-80 mg/24 hrs (as rest) or 1-14 mg/dL
Up to 250 mg/24 hr following exercise
Albumin 37.9%
α1 globulin 27.3%
 Annexure 1: Normal Laboratory Values 337

α2 globulin 19.5%
β globulin 8.8%
γ globulin 3.3%
Negative by qualitative test up to 0.5 g/24 hr by quantitative test
Galactose
Neonate < 60 mg/dL
Children 14 mg/24 hrs
Sodium in 24 hr sample
40-220 mmol (diet-dependent)
Potassium in 24 hr sample
2.5-125 mmol/L (diet-dependent)
Calcium in 24 hr sample
5-150 mg (diet-dependent)
Chloride in 24 hr sample
Infants 2-10 mmol (diet-dependent)
Children 15-40 mmol
Urinary creatinine
Preterm 8-15.0 mg/kg/24 hr
Term 10.4-19.7 mg/kg/24 hr
1-7 yr 10-15.0 mg/kg/24 hr
7-15 yr 5.2-41 mg/kg/24 hr
Creatinine clearance (endogenous)
Newborn 40-65 mL/min/1.73 m2
Children
Male 97-137 mL/min/1.73 m2
Female 88-128 mL/min/1.73 m2
Ammonia nitrogen
50-120 mgN/24 hr
Urinary Copper
0.36-7.56 mg/mol creatinine
Urinary Coproporphyrin
34-234 μg/24 hr
Total Free Catecholamines
0-1 yr 10-15 g/24 hr
1-5 yr 15-40 g/24 hr
6-15 yr 20-80 g/24 hr
Homovanillic acid(HVA)
0-1 yr < 32.2 mg/g creatinine
2-4 yr < 22 mg/g creatinine
5-19 yr < 14 mg/g creatinine
Vanillylmandelic acid (VMA)
0-1 yr < 18.8 mg/g creatinine
2-4 yr < 11.0 mg/g creatinine
5-19 yr < 8.0 mg/g creatinine
Mucopolysaccharides
0-2 yr < 50 μg/g creatinine
2-4 yr <25 μg/g creatinine
Hemoglobin, bilirubin, ketones, myoglobin, phorphobilinogen and glucose are
undetectable in normal urine by qualitative tests.
338 Selected Topics in Pediatrics for Practitioners

CEREBROSPINAL FLUID
Volume
Adult 100-160 mL
Child 60-100mL
Pressure
70-180 mm water
Cell count (in per cu mm)
Preterm Term Neonate Thereafter
Lymphocytes 0-25 0-20 0-5 0-5
Polymorphs 0-10 0-10 0-10 nil
Red blood cells 0-1000 0-800 0-50 nil
Proteins (in mg/dL)
Total 40-300 45-120 40-120 10-20
Glucose (in mg/dL)
50-70 percent of corresponding blood sugar
Chloride
118-132 mmol/L

STOOL SPECIMEN
Fecal pH 7.0-7.5
Fecal Fats (measured over 72 hrs)
Breastfed infants < 1 g/24 hr
0-6 yr < 2 g/24 hr
Fecal Bile Acids
120-225 mg/24 hr
Fecal α 1 Antitrypsin
Breastfed infant < 4.4 mg/g stool
Top fed infant < 2.9 mg/g stool
6 mo-4 yr < 1.7 mg/g stool
Occult Blood
Negative, i.e., <2 mL per 24 hrs in 100-200 matter
Ova and Cyst
Nil

AMNIOTIC FLUID
α Fetoprotein
Gestational Mean level
15 13.5 ± 3.42 μg/mL
16 11.7 ± 3.38 μg/mL
17 10.3 ± 3.03 μg/mL
18 9.5 ± 3.22 μg/mL
19 7.1 ± 2.85 μg/mL
20 5.0 ± 2.45 μg/mL
Creatinine
> 2.0 mg/dL after 37 weeks of gestation
Lecithin
> 0.10 mg/dL indicates fetal lung maturity
Lecithin/sphingomyelin ratio (L/S)
2-5 indicates fetal lung maturity
 Annexure 1: Normal Laboratory Values 339

Total bilirubin
Gestational age
28 weeks < 0.075 mg/dL
40 weeks < 0.025 mg/dL

SWEAT
Sweat chloride
Borderline 40-60 mmol/L
Normal < 40 mmol/L
In cystic fibrosis, values are greater than > 60 mmol/L

SERUM VITAMIN LEVELS

Vitamin A (retinol)
0-1 yr 20-43 µg/dL
2-4 yr 25-48 µg/dL
5-19 yr 26-72 µg/dL
β Carotene
0-1 yr 20-70 ug/dL
children 40-130 ug/dL
Vitamin B1 (thiamine)
0-2.0 µg/dL
Vitamin B2 (riboflavin)
1-3 yr 500-900 µg/g creatinine
4-6 yr 300-600 mg/g creatinine
7-9 yr 270-500 mg/g creatinine
10-15 yr 200-400 mg/g creatinine
Vitamin B6 3.6-18 ng/mL
Vitamin B12
Newborn 175-800 pg/mL
Children 140-700 pg/mL
Serum Folate
Newborn 7.0-32 ng/mL
Children 1.8-9 ng/mL
Vitamin C
0.6-2.0 mg/dL
Vitamin D (25-hydroxy)
1 month to 1 year 7.4-53 ng/mL
1,25-hydroxy 25-45 pg/mL
(1,25-hydroxy)
calcitriol
Vitamin E
1-6 yr 3.0-9.0 mg/L
7-19 yr 4.4-10.4 mg/L
 Annexure 2
Fluid Therapy
Ramesh Santhanakrishnan

The understanding of the principles of fluid and electrolyte balance is vital for the
maintenance of stable internal environment. This is even more essential in infants
who have less reserves of body water and electrolytes and in newborn babies who
may be deficient of the homeastatic mechanism to protect them against the changes
realted to abnormal losses. Thus, it is important to assess the nature and magnitude
of any distrubance in different clinical situations and at different ages because
correction of the imbalance is essential for speedy recovery.
Before venturing into the abnormal related to various diseases, it is necessary to
understand the physiological aspects of body water and electrolytes, why infants are
more vulnerable to pathological changes in any altered clinical situation, and why the
mortality is likely to be more in young infants compared to older children and adults.
1. Very young infants are vulnerable to more water loss because of physiological
inability of their renal tubules to concentrate.
2. Higher metabolic rate and larger surface area compared to total body weight in
young infants favour rapid fluid loss. Unless fluids are adequately replaced in
the presence of continued loss, dehydration and consequences of dehydration
are likely to set in.
3. Larger turnover is another problem in young infants. An infant exchanges about
one-half of his or her ECF everyday compared to one-seventh in an adult.
4. Thirst mechanism is very effective in older children and adults compared to very
young infants. In the presence of excessive water loss, young infants do not
express their thirst for fluids effectively when there is a negative balance of
intake during water loss.

TOTAL BODY WATER

The proportion of body water content varies with age and adipose tissue. Neonates
have relatively large water content compared to adults. Likewise, those who are
obese have less water content. The water content is around 80 percent in neonates
as compared to nearly 60 percent in adolescents and adults.
Distribution of body water The intracelluar fluid is separated by a cell wall from
extracellular fluid which is further subdivided into intravascular and extravascular
compartments.
Fluid intake and water balance Maintenance needs of body fluids is to provide an
equilibrium between intake and output.
Body fluids different compartments average
Infant (3 kg) (0.2 mf) Adult 70kg (1.85 Mg)
%Body wt. Ltr. Liters/Mf %Body wt. Ltrs Ltrs/Mf
Intracellular 38 1.14 5.70 40 28.0 15.2
Extracellular 33 0.99 4.55 16 11.2 6.0
Interstitial plasma 5 0.15 0.75 4 2.8 1.5
Total 76 2.28 11.00 60 42.0 22.7
 Annexure 2: Fluid Therapy 341

Water Loss
Water loss mainly occurs through lungs, skin, urine and motion.
There are many factors which affect water balance. These include body
temperature, environmental temperature, humidity, etc.
Electrolyte composition: The composition of extra cellular fluids is easily analyzed, the
greater part of it is plasma. ECF contains more of sodium, poor in potassium—
whereas ICF primarily contains mostly potassium, protein andphosphate. The table
provides the different cations and anions in plasma.
Different cations and anions in plasma
Cations mEq/L Anions mEq/L
Sodium 140 Chloride 109
Potassium 4 Bicarbonate 18
Calcium 5 Protein 15
Magnesium 2 Phosphate 3
Organic acids 6
Total 151 151

Normaly, plasma water accounts for approximately 93 percent of the plasma

volume and there will be variations in the electrolytes concentration-in the presence
of hyperlipidemia, hyperglycemia.

Intracellular Fluid (ICF)

Intra cellular fluid contains high concentration of potassium and to some extent
magnesium. It is difficult to quantify or analyze ICF in routine management. Though
the sum of anions and cations are greater than ECF, normal osmotic equilibrium
maintained between ECF and ICF by diminished particle, i.e. one osmotic particle
from the excess of divalent and polyvalent anions—and some given univalent ions
especially potassium are not in free ionic form but in combination with anions, thus,
reducing the actual number of osmotic particles.
Before venturing into the abnormals related to various disease states, the normal
physiology and the scientific basis of maintenance of fluid must be understood
clearly.
Intracellular Fluid
Cations mEq/L Anions mEq/L
Sodium 9 Chloride 4
Potassium 158 Bicarbonate 10
Calcium 3 Protein 65
Manesium 30 Phosphate 95
Sulfate 22
Organic acids 4
200 200

Maintenance Therapy
Fluid and electrolyte requirements are directly related to metabolic rate and calorie
intake. Many methods of calculating the maintenance of fluids have been advocated.
Weight, calorie expanded, or surface area alone will not be accurate over range of
342 Selected Topics in Pediatrics for Practitioners

ages or size, but calorie expenditure related to body weight is a simplified method.
The newborn and few other states like obesity and edema are exceptions to a surface
area relationship. Using value for calorie expenditure at basal conditions from the
Table gives an idea regarding the approximate basal needs.
Approximate basal needs in relation to age, weight and surface area
Age Weight in kg Surface area m2 Maintenance basal
water requirements
ml/kg or cal/kg
Newborn 2.5-4 0.2-0.23 50
1wk to 6 m 3-6 0.2-0.35 65-70
6m-12 mon 6-10 0.35-0.45 50-60
12m-2 yrs 10-12 0.45-0.6 45-60
2 yrs-10 yrs 40-50

The maintenance needs will be 1½ times the basal needs taking into consideration
the activity, temperature variations, rate of breathing, coupled with observed urine
formation High fever, hyperventilation, etc. may increase the basal needs 2 to 3
times.
Another similar method for calculating calorie expenditure from body weight is
given in the table.
Calculation of calorie expenditure from body weight
Body wt. Calorie expenditure/day Approx.fluid needs
Up to 10 kg 100 kcal/kg 100ml/kg
11-20 kg 1000 kcal + 50 kcal for each kg above 10 80-100 ml/kg
Above 20 kg 1500 kcal + 20 kcal for each kg above 20 60-80 ml/kg
And above 30 kg 60 ml/kg

In neonates the fluid needs are far less in the first week of life, 60-65 ml/kg in
the first 2 to 3 days life is adequate and gradually inceased to 100 ml/kg after a
week.
The following points must be kept in mind while formulating fluid therapy for
neonates, infants and children. When the child is not in a fit condition to accept oral
feeds, parenteral fluid therapy must be considered as the alternated method of
providing water and electrolytes. The water requirements have been discussed already
on the basis of “rule of the thumb” calculation.
1. Weight in kg is better than surface area or calorie requirements per kg.
2. Eighty to one hundred ml/kg will be the fluid needs for maintenance in children
within the ages of 1 week to 1 month.
3. In the first week of life, the fluid requirements will be in the range of 60-90 ml/
kg.
4. After the age of 1 to 2 years, the needs will be 80 ml/kg.
5. Older children will need, beyond the age of 4 years, 60-80 ml/kg.
6. Any rehydration fluid must contain 5 percent Dextrose except in diabetes mellitus
where it has to be decided individually.
7. Glucose (10%) in distilled water will be ideal for neonates.
8. The neonates do not usually require Na+ or K+ in the first 48 hours except in
the presence of continued loss from GI system.
9. Na+ needs are 2-3 mEq/kg/24 hrs or 20-25 mEq/L of any maintenance fluid.
10. Any continued loss of Na+ must be replaced adequately.
 Annexure 2: Fluid Therapy 343

11. Correction of Hyponatremia (135-X) x 0.6 x weight in kg = mEq of Na required

(X is the actual sodium level observed).
Symptomatic hyponatremia: Use hypertonic saline (3% sodium chloride provides 0.5
mEq/ ml) to deliver approximately 6 mEq/kg/hr (12ml if 3% NaCl/kg/hr). This
usually raises the sodium level by 10 mEq/L. The initial rapid correction to raise
the sodium level is only be to a value of about 125 mEq/L. If the child is convulsing
3 ml/kg may be given as a rapid infusion over a period of 10-15 minutes. Following
acute corection, if the child’s acidosis worsens, replace part of the sodium (nearly
1/4th of Na deficit) as sodium bicarbonate (0.9 mEq/ml). Subsequent elevation of
sodium levels should be affected in small increments.
Asymptomatic hyponatremia: The entire sodium deficits can be replaced as 5 percent
GNS (15 mEq/100ml) seperately or can be given along with pediatric maintenance
solution (If the child is avoiding urine adequately).
Hypernatremic dehydration: The sodium deficit is relatively small and extracellular
fluid volume is well-maintained. It will be adequate to provide a 5 percent Dextrose
solution containing 25 mEq/L of sodium. Sodium-free solutions are likely to
precipitate seizures.
12. The K+ maintenance needs are 2 mEq/kg or 20 mEq/L of pediatric maintenance
fluid. In the presence of hypokalemia, potassium replacements must be done
slowly over a period of 48 to 72 hours provided the child has adequate urine
output. No fluid should contain more than 30mEq/L or rarely up to 40 mEq/
L. Not more than 4 mEq/kg can be given in the course of 24 hrs. The risk of
K+ toxicity is much more than the risk of moderate hypokalemia.
13. Bicarbonate deficiency must be corrected partially and that to if the child is
clinically symptomatic and the value is less than 10 mEq/L in the presence of
metabolic acidosis.
14. Metabolic alkalosis associated with volume contraction responds to measures
designed to expand volume and replacement of the chloride and potassium
deficit. Otherwise the therapy must be directed to the underlying cause.
15. Respiratory acidosis where pH is markedly lowered due to retention of carbon
dioxide as insevere respiratory insufficiency. Apart from blood gas and pH
assessment, appropriate treatment is directed to improve ventilation. Sodium
bicarbonate administration may precipitate cardiac failure.
16. Respiratory askalosis if any, associated with CNS disease, severe hypoxia, etc.,
should be corrected by appropriate measures of removing underlying cause.
17. Disturbed metabolism of fluid and electrolutes in other altered clinical states must
be understood properly, and plan of therapy must be based according to the
cause of the abnormalities, whether it is related to metabolic renal, respiratory,
CNS, etc.
 Annexure 3
Drugs and Drug Dosage
Ramesh Santhanakrishnan

The drugs and drugs dosage in pediatric practice given in this annexure is not
exhaustive. The dosage recomended are precise and in agreement with standards
officially accepted -the dosage schedule may change from time to time in the light
of continued clinical experience. Drugs recommended now may be banned or
contraindicted in children at a later date. Check the manufacture’s recommendations
if the drug is occasionally prescribed.

ANTIBIOTICS
Aminoglycosides
Amikacin
7.5 mg/kg—single or 2 div doses IM/IV for newborn under 7 days.
15.0 mg/kg/24 hrs in 2 div doses IM/IV.
20 mg/kg/24 hrs in serious infections and neonatal meningitis.

Gentamicin Sulfate
3-5 mg/kg/24 hrs in serious infections and neonatal meningitis. Individualized
according to weight, renal function and gestational age lesser dose of 3-4 mg/kg for
neonates under 7 days weighing 800-2000 gm.
Note: Dose of gentamicin has to be adjusted according to serum creatinine levels in
the presence of renal failure. Serum creatinine × 9 hrs = interval between 2 doses
in hrs.

Streptomycin Sulfate
20 mg/kg/24 hrs IM as a single dose.

Sisomycin Sulfate
5-6 mg/kg/24 hrs IM in div doses in neonates.
3-5 mg/kg/24 hrs IM in 2 div doses in infants and children.

Tobramycin
4-6 mg/kg/24 hrs IM/IV in 2 or 3 div doses.

Netilmicin Sulfate
5-7.5 mg/kg/24 hrs IM/IV in 2 or 3 div doses (up to 7.5 mg/kg/24 hrs in severe
infections for the first 48 hrs)
 Annexure 3: Drugs and Drug Dosage 345

Penicillin
Benzyl Penicillin (Penicillin G)
50,000 units/kg/24 hrs in 2 div doses IM/IV for preterm and term neonates.
25,000 to 50,000 units/kg/24 hrs in 4 div doses IM/IV for older children.
100000 to 150,000 units/kg/24 hrs IV in 2 div doses for neonates under 7 days
of age (for serious infections).
150,000 to 200,000 units/kg/24 hrs IV in 3-4 div doses for neonates between 8-
28 days (for serious infections).
250,000 to 400,000 units/kg/24 hrs IV in 4-6 div doses for infants and children
in pyogenic meningitis.
200,000 to 250,000 unit/kg/24 hrs IV in 4 div doses for 7 days in leptospirosis.

Penicilin “G” Procaine

25,000 to 50,000 units/kg/24 hrs single dose IM (avoid in neonates)

Penicillin “G” Benzathine

0.6 to 1.2 million units IM.

Oral Penicillin
25,000 to 50,000 units/kg/24 hrs in 4 div doses given 1 hour before meals or 2 hours
after meals.
(200,000 units = 125 mg of phenoxy methyl penicillin).

Betalactamase-Resistant Penicillin
Cloxacillin 50 to 100 mg/kg/24 hrs IV/IM /oral, in 4 div doses (oral—1 to 2 hrs
before meals).
25 mg/kg/24 hrs in newborn.
Methicillin 100mg/kg/24 hrs IV/IM in 6 div doses for mild infections.
200 mg/kg/24 hrs for severe infections.
50 mg/kg/24 hrs in neonates.
Naficillin 25 to 50 mg/kg/24 hrs IV/IM in 4 to 6 div doses.
30 to 40 mg/kg/24 hrs (0) in neonates.
100 to 200 mg/kg/24 hrs IV in meningitis
Oxacillin 50 to 100 mg/kg/24 hrs IM in infants over 1-2 weeks of age.
150-200 mg/kg/24 hrs in older infants and children.

Modified Penicillins
Ampicillin
50 to 100 mg/kg/24 hrs in 4 div doses IM/IV/oral in moderate infections.
150 to 200 mg/kg/24 hrs in 4 div doses IM/IV in severe infections.
100 to 200 mg/kg/24 hrs IV in neonatal meningitis (0-28 days).
200 to 300 mg/kg/24 hrs in 4 div doses Iv for very severe infections like pyogenic
meningitis (in infants and older children).

Ampicillin with Sulbactam

50-100 mg/kg/24 hrs of ampicillin in 3 div doses preferrably as Iv infusion over 20-
30 mts.
346 Selected Topics in Pediatrics for Practitioners

Use injectables within an hour of reconstitution.

Avoid prolonged Iv drip owing to loss of 10 percent activity in 4 hrs. If given
by direct IV, give slowly over 10 minutes (maximum dose: 2g/day).

Carbenicillin
200 mg/kg/24 hrs IM/IV in 2 div doses—first week of life.
300 mg/kg/24 hrs IM/IV in 3 div doses—beyond first week of life.
400 to 500 mg/kg/24 hrs IM/IV in 6 div doses for severe infections
(Pseudomonas infection).

Hetacillin
25 to 40 mg/kg/24 hrs oral, IM/IV.

Amoxycillin
25-40 mg/kg/24 hrs (O) in div doses.
40 to 50 mg/kg/24 hrs (O) in 3 div doses for older children (20 kg and more).
50 mg/kg/24 hrs IV every 8 hours.

Amoxycillin with clavulanic acid

20-40 mg/kg/24 hrs of amoxycillin + 5 to 10 mg/kg if clavulanic acid (oral) in 3 div
doses, twice daily in neonates under 7 days (useful in otitis and sinusitis).
25 mg/kg of Amox + 5 mg of Cl acid/kg/24 hrs IV in 3 div doses.

Ticarcillin
50 to 100 mg/kg/24 hrs, IV/IM in 3-4 div doses.
200 to 300 mg/kg/24 hrs IV for serious infections.

Piperacillin
50 to 100 mg/kg/24 hrs IV/IM in 3-4 div doses.
200 to 300 mg/kg/24 hrs IV for serious infection.

Mezlocillin
150-300 mg/kg/24 hrs IV every 12 hrs for neonates (under 7 days).
200-300 mg/kg/24 hrs IV every 6-8 hrs for neonates (more than 7 days).
300-450 mg/kg/24 hrs IV every 4-6 hrs for infants and children.

Azlocillin
150-300 mg/kg/day IV every 8 hr for neonates.
300-450 mg/kg/day IV every 4 hr for infants and children.

Becampicillin
25-30 mg/kg/day every 2 hrs oral.

Cephalosporins
First Generation
1. Cephalexin 25-30 mg/kg/24 hrs in 3 div doses (O).
 Annexure 3: Drugs and Drug Dosage 347

2. Cefadroxil 30 mg/kg/24 hrs in 2 div doses (O).

3. Cefazolin 40 mg/kg/24 hrs in 2 div doses IVIM (newborn)-IV given over 15-30
min 50-100 mg/kg/24 hrs IMIV in 4 div doses (Children)

Second Generation
1. Cefaclor 20-40 mg/kg/24 hrs in 3 div doses (O).
2. Cefuroxime 20-30 mg/kg/24 hrs (O).
3. Cefuroxime 50-100 mg/kg/day in 3-4 div doses IM/IV (infants over 3
months). (Max. 240 mg/kg/24 hrs) 100 mg/kg/day in 3 div
doses IV (neonatal meningitis).
4. Cefoxitin 80-160 mg/kg/24 hrs IV/IM in 4-6 div doses.
5. Cefamandole 50-150 mg/kg/24 hrs IV/IM in 4-6 div doses.
6. Cefoxitin 80-160 mg/kg 24 hrs IV in 4-6 div doses.

Third Generation
1. Cefixime 8mg/kg/24 hrs (O) single or 2 div doses.
2. Cefoperazone 50-200 mg/kg/24 hrs in 2 div doses (IM/IV).
3. Cefotaxime 100 mg/kg/24 hrs in 2 div doses (0-1 week).
150 mg/kg/24 hrs IV in 3 div doses (1-4 weeks).
100-150 mg/kg/24 hrs IM/IV in 4 div doses in infants and
children. 200 mg/kg/24 hrs IV 4 div doses in bacterial meningitis
4. Ceftazidime 50-100 mg/kg/24 hrs IV in 2 div dose (under 2 kg).
100 mg/kg/24 hrs 3 div doses (over 2 kg).
100-150 mg/kg/24 hrs IV 3 div doses in infants and children.
5. Cefpodoxime 10 mg/kg 24 hrs (O) in 2 eiv doses.
6. Ceftibuten 9 mg/kg/24 hrs (O) in a single dose
7. Ceftizoxime 30-60 mg/kg/24 hrs in 2 or 3 div doses (infants over 3 months).
100-150 mg/kg/24 hrs in 2 or 3 div dose in life-threatening
infection (max up to 200 mg/kg).
8. Ceftriaxone Children—50-75/kg IM Q 24 hrs. IV q 24 hr or Q 12 hr.
Meningitis 75 mg/kg dose 1 then 80 100 mg/kg/day divided
q 12-24 hr 18-100 mg/kg/24 hrs in meningitis div every 12 hrs
(max/4g).

Macrolides and Related Drugs

Clindamycin 10-25 mg/kg24 hrs (O) in 4 div
Palmitate dose
Clindamycin 25-50 mg/kg 24 hrs IM/IV in 3-4 div
Phosphate doses.
Lincomycin 30-60 mg/kg/24 hrs (O) in 3 div doses.
Spiramicin 0.15-0.3 mIU/kg/24 hrs (O) in 2 div doses.
Roxithromycin 5-10 mg/kg/24 hrs (O) in 2 div doses.
Erythromycin 20-40 mg/kg/24 hrs (O) in 3-4 div
(Estolate Stearate) doses.
Ethylsuccinate 40 mg/kg/24 hrs (O) in 3-5 div doses.

Tetracyclines
Avoid in children under 8 yrs of age
Tetracycline 20-40 mg/kg/24 hrs (O) in 4 div doses.
348 Selected Topics in Pediatrics for Practitioners

Oxytetracycline Preferrably given an hour before feeding.

10-20 mg/kg/24 hrs IM/IV in 2 or 3 div doses-painful and
achieves poor level with IM injections.
Doxycycline 4.4 mg/kg/(O) initially, then 2.2 mg/kg (O) subsequent days
as a single dose.
Minocycline 4 mg/kg in 2 div doses(O).
Demeclocycline 6-12 mg/kg/24 hrs in 2 div doses(O).

Vancomycin
30 mg/kg/24 hrs in 2 div doses IV given over a period of one hour (in neonates
under 7 days).
40 mg/kg/24 hrs in 3 div doses IV with start dose of 15 mg/kg (for neonates
between 7-30 days).
40 mg/kg/24 hrs in 4 div doses IV an infants and children (10 mg/kg/dosess)—
(diluted in 30 ml, water) every 6 hrs (O) in Cl. Difficile pseudomembranous colitis.

Fluoroquinolones
(preferably avoided under 12 years)
Norfloxacin 6-12 mg/kg/24 hrs (O) in 2 div doses (up to 7 days in UTI).
Ciprofloxacin 10-15 mg/kg/24 hrs (O) in 2 div doses.
5-10 mg/kg/24 hrs IV in 2 div doses given over 30 mts.
Ofloxacin 10 mg/kg/24 hrs (O) in 2 div doses. 5-10 mg/kg/24 hrs IV in
2 div doses.
Pefloxacin 12 mg/kg/24 hrs (O) in 2 div doses. 5-10 mg/kg/24 hrs IV in
2 div doses.

ANTITUBERCULAR DRUGS
Drugs Single daily doses given in an empty stomach
Isoniazid (H) 5 mg/kg/day (O)
(max 300 mg/day)
Rifampicin (R) 10 mg/kg/day (O)
Streptomycin (S) 15-20 mg/kg/day IM (max 1.0 g daily)
Pyrazinamide 25-30 mg/kg/day (O)
Ethambutol (E) 25 mg/kg/day (O) for 6-8 weeks. 15 mg/kg/day thereafter.

Less Freqently used Antitubercular Drugs in Children

Thiacetazone 4 mg/kg/day.
PAS sodium 300 mg/kg/day.
Cycloserine 15 mg/kg/day.
Capromycin 15 mg/kg/day.
Ethionamide 15-20 mg/kg/day.
Kanamycin 10-15 mg/kg/day.

Chemotherapeutics
Furazolidine
5 to 6 mg/kg/24 hrs (O) in 4 div doses
8 to 10 mg/kg/24 hrs (O) in enteric fever.
 Annexure 3: Drugs and Drug Dosage 349

Methenamine Mandelate
100 mg/kg/24 hrs initially 50 mg/kg/24 hrs afterwards.
Nalidixic Acid
50 to 60 mg/kg/ 24 hrs (O) in 4 div doses for suppressive therapy in UTI: 2.5
mg/kg/24 hrs.
Nitrofurantoin
5 to 7 mg/kg/24 hrs (O) in 4 div doses for 10 to 14 days. Half dose—beyond
10 to 14 days. Quarter dose—after another 10 to 14 days.
Sulfonamides
1. Sulfadiazine—150 mg/kg/day in div doses (max 3 gm/day).
2. Sulfisoxazole—120 to 150 mg/kg/24hrs in 4 div doses half of total dailydose to
be given initially.
3. Sulfamethoxazole (SMZ) with trimethoprim (TMP) SXZ—30 mg/kg/24 hrs (max
40 to 50 mg/kg/TMP—6 mg/kg/24 hrs (max 8 to 10 mg/kg (O) in 2 div doses).
Metronidazole IV (for anaerobic infections) 500 mg/100 ml (5 mg/ml).
7.5 mg/kg every 8 hours IV as an infusion.
15 mg/kg/as loading dose in CNS infection.
7.5 mg/kg every 12 hours in neonates, avoid during the first four days of ife.

ANTIMALARIALS
Chloroquine (base 150 mg of 250 mg tab)-10 mg/kg loading dose followed by 5 mg/
kg 6 hrs, later on day 1 and 5 mg/kg as single dose for the next 2-3 days. (5 mg/
kg IM as a single dose repeat 6 hrs later (not to exceed 10 mg/kg/24 hrs).
Primaquine – 0.3-0.4 mg/kg (max 15 mg) as a singledose (base equal to 0.55 mg salt)
daily for 14-21 days.
Quinine Sulfate – 15-25 mg/kg/24 hrs (O) in 3 div doses for 7-10 days or 20 mg/
kg/IV over 4 hours, then 7.5 mg/kg/dose every 8 hrs (IV given over 1 hr) for 2-
3 days, later 8-10 mg/kg/dose every 8 hrs (oral – for 5 days).
Pyrimethamine (25 mg) with sulfa methopyrazine 500 mg or Sulfadoxine—1 mg/kg/ of PM
+ 20 mg/kg (SMO/SD) as a single dose.
Mefloquine—15 mg/kg single dose (max 750 mg) followed by 10 mg/kg 6-8 hrs later,
as prophylaxis—5 mg/kg (max 250 mg) weekly once.
Artesunate (Falcigo)—10-12 mg/kg (O) divided over 7 days.
Artemether—1m 3.2 mg/kg IM stat. Followed by 1.6 mg/kg/day till oral therapy possible.
Oral same regimen as for artesunate.

ANTIAMOEBIC DRUGS
Metronidazole—30 to 50 mg/kg/24 hrs (O) in 3 div doses for 7 to 10 days.
Tinidazole—20 to 30 mg/kg/24 hrs (O) in 2 div doses for 5 days.
Diloxanide furoate—20 mg/kg/24 hrs (O) in 3 div doses for 10 days.
Di-iodohydroxyquin—40 mg/kg/24 hrs (O) in 3 div doses for 20 days (occasionally used).
1. Emetine hydrochloride—1mg/kg/day IM for 5 days rarely used.
2. Dehydroemetine HCL—1.5 mg/kg/day IM for 5 days (useful in life-threatening
dysentery)
3. Secnidazole—30 mg/kg single or div doses (single day therapy).
350 Selected Topics in Pediatrics for Practitioners

ANTIGIARDIASIS DRUGS
Metronidazole—15-20 mg/kg/24 hrs (O) in 3 div doses for 5 to 7 days.
Furazolidone—5 mg/kg/24 hrs (O) in 3 div doses for 7 days.
Tinidazole—15-25 mg/kg/24 hrs (O) in 3 div doses for 5 to 7 days.

ANTHELMINTICS
Piperazine citrate—75 mg/kg/24 hrs as a single dose for 2 consecutive days (max 3 gm/
24 hrs). 65 mg/kg/24 hrs (max 2.5 gm/24 hrs) for 8 days, for enterobiasis (pinworm). Repeat
after one week.
Pyrantel pamoate—10mg/kg as a single dose for ascariasis, enterobiasis and ankylostomiasis.
Mebendazole—100 mg twice daily for 3 days, for ascariasis, ankylostomiasis, trichuriasis
and strongyloidiasis. 100 mg as a single dose is adequate for enterobiasis. Repeat after 3
weeks.
Albendazole—400 mg single dose, 200 mg for children between 1-2 years.
Praziquantel—50 mg/kg/24 hrs in 3 div doses for 14 days for cysticercosis

CARDIOVASCULAR DRUGS
Digoxin
1. 0.02 to .025 mg/kg (O) as total digitalizing dose and 0.005 mg as maintenance
digitalising dose in preterm.
2. 0.03-0.05 mg/kg as digitalizing dose and 0.01-0.15 mg/kg as maintenance in
term neonates and children Half the digitalizing dose is given initially as stat
dose and the other half in 2 divided doses every 6 to 8 hours. Parenteral
digitalizing dose—75 percent of oral given as IV.
Propranolol 0.3 to 1.2 mg/kg/day (O) in 3 div doses. 0.01 to 0.1 mg/kg/
dose IV over 10 mins. Repeat every 20 minutes if needed (for
supraventricular tachycardia).
Hydralazine 2 to 4 mg/kg (O) in div doses (in refractory congestive cardiac
failure).
Diazoxide 2 mg/kg/dose (max 10 mg/kg/dose).
Isoproterenol 0.05-0.2 mg/kg/min 1mg in 250 ml of 5% GDW provides 4
mg/ml
Dopamine 5-10 mg/kg/min (useful in presence of low arterial pressure
and cardiac output).
Potassium chloride Potassium chloride solution 15 ml contains 20 mEq of potassium.
Quinidine sulfate 2-10 mg/kg/dose every 4-6 hours (loading dose), 30 mg/kg/
day in 4 div doses (max 2g) as maintenance.
Quinidine gluconateLoading dose—as needed: 30 mg/kg/day in 4 div doses as
maintenance.
Procainamide 0.4 mg/kg/min for max 23 min then 20 80 mcg/kg/min. Oral—2-8
mg/kg dose 4 hrly
Lidocaine 1 mg/kg IV repeat every 5 min x 3 doses (loading dose): 0.02-
0.05 mg/kg/min 5 mg/kg/24hrs.) as maintenance.
Propranolol 0.1-0.15 mg/kg (loading dose): 1-4 mg/kg/day in 4 div doses
as maintenance.
Atropine sulfate 0.02 mg/kg (max 0.6 mg) IV or IM then 0.01 mg/kg/dose 4-
6 H.
AmiodaroneHCL 10 mg/kg/24 hrs (O) in 2 div doses (maintenance).
 Annexure 3: Drugs and Drug Dosage 351

ANTIHYPERTENSIVE DRUGS
Sodium nitroprusside 0.5-10 μg/kg/minute
Methyldopa 10-40 mg/kg/day (O) in 2-3 div doses.
Nifedipine (1) 0.2-0.5 mg/kg/dose sublingual for hypertensive emergency.
(2) 1-2 mg/kg/day (O) q 6 hrly. NB: substained release forms
are given q 12 hr. Dosage remains same.

Captopril
1. <2 mo: Initial starting dose: 0.1-0.25 mg/kg/dose q 8-24 hr Titrate dose up to
0.8 mg/kg/dose Q6-24 hr
2. >2 mo: Initial starting dose 0.5 mg/kg/dose. Titrate to a maximum of 6 mg/kg/
day in 1-4 doses of 75 mg/day.

BRONCHODILATORS
Adrenaline (1:1000 aqueous): 0.01 ml/kg/dose SC Max: 0.3 ml repeat 20 min later.
Ephidrine 3 mg/kg/24 hrs every 6 hrs (4 div doses).
Deriphyllin 3-4 mg/kg/dose (O) IM/IV
Aminophyline 3-4 mg/kg/dose IV every 6 hr
Salbutamol 0.1-0.15 mg/kg/dose every 6 hr (max 6 mg/day).
Terbutaline 0.1-0.15 mg/kg/dose every 6 hr (max 5 mg/day) 0.005 mg/kg.
Sc (max 0.3 mg)
Orciprenaline 1.5-2 mg/kg/24 hr (O) in 3 or 4 div doses.
Predinisolone 1mg/kg/24 hr in 3 div doses (4-5 days)

ANTIFUNGAL DRUGS
Amphotericin B 0.25 mg/kg IV initially, infuse as a single dose in 4 to 6 hours.
Dilution—0.1 mg/ml in 5% GDW. First test dose 0.1 mg/kg
and the therapeutic dose is given on the same day. Dose
increased in daily increments of 0.1 to 0.25 mg/kg during a 4-
day period until a total dose of 0.5 to 1.0 mg/kg is reached.
Griseofulvin Microsize 10-12 mg/kg/(O) in 2 div doses. Ultramicrosize 5.0 mg/kg
single dose.
Mycostatin (Nystatin) 200,000 units 4 time/day for infants (O), 400,000-600,000 units
4 times/day for children and adults.
Miconazole 20-40 mg/24 hrs IV in 3 div doses infused over 30-60 minutes.
Ketoconazole 3.5 mg/kg/24 hours (O)—as a single dose, then 2 mg/kg/day
(7-14 days).

ANTIVIRAL DRUGS
Acyclovir (zovirax) Genital herpes simplex virus (HSV) infection—200 mg, 5 times
daily oral for 10 days or 1.5 mg/kg/day IV in 3 divided doses
for 5-7 days.
Amantadine HCI Influenza A virus infection—4.4 mg/kg/(O) in 2 div doses 1-
9 years for 2-7 days, 200 mg/day (O) in 2 div doses above 9
years weighting more than 45 kg for 2-7 days.
Ribavirin In RSV infection—an aeorsal in a solution containing 20 mg/
ml for 12-18 hrs/day for 3-7 days (limited usefulness). In chronic
hepatitis C—10 mg/kg/day (O) for 5-10 days.
352 Selected Topics in Pediatrics for Practitioners

Ganciclovir Antiviral agent used for prophylaxis and treatment of

cytomegalovirus infections: (slow IV infusions—1 hr). Initial
therapy (induction) 10 mg/kg/24 hours, div every 8-12 hours
for 14-21 days. Maintenance therapy 5-6 mg/kg/ over 1 hour
daily (reduce dose in renal impairment).

ANALGESICS AND ANTIPYRETICS

Acetaminophen 40-65 mg/kg/24 hours (O) in 4 div doses (lower dose in hepatic
disease).
Paracetamol 40-65 mg/kg/24 hours (O) in 4 div doses (lower dose in hepatic
disease)
Mefenamic acid 20 mg/kg/24 hrs (O) in 3 div doses.
Nimesulide 5 mg/kg/24 hrs (O) in 3 div doses.

NONSTREROIDAL ANTI-INFLAMMATORY DRUG (NSAIDS)

(Avoid in asthmatic children)
Aspirin 70-100 mg/kg/24 hrs (O) in 4-6 doses
Ibuprofen 10-15 mg/kg/dose (O) lat intervals of 4-6 hr (max 40-60 mg/
kg/24 hrs).
30-70 mg/kg/24 hrs in rheumatiod arthritis in 4-6 div doses.
Naproxen 10 mg/kg/24 hrs (O) in 2-3 div doses.
Ketoprofen 2 mg/kg/24 hrs in 3 div doses.
Piroxicam 1-2 mg/kg/24 hrs in 2 div doses.
Zolmetin sodium 15 mg/kg/day with increase of 5 mg/kg/day at weekly
intervals until efficacy is noted.
Gold Initial 10 mg/kg (up to 50 mg) IM of gold sodium thiomalate as a
weekly injection, given over a long period. Response will not
be seen for 3-4 months.
Indomethacin 1-3 mg/kg/24 hrs (O) Max up to 100 mg in 2-3 div doses.
Single dose of 1 mg/kg at night for early morning stiffness.
Ketorolac 1-2 mg/kg/24 in 2 div doses.
Tenoxicam 0.2-0.4 mg/kg/24 hrs (max 20 mg) (O) in 4 div doses

ANTIHISTAMINICS
Chlorpheniramine
maleate 0.35 mg/kg/24 hrs (O) in 4 div doses.
Cyprohepatadine
HCL 0.25 mg/kg/24 hrs (O) in 4-6 div doses.
Dexchlorpheniramine
maleate 0.15 mg/kg/24 hrs (O) in div doses.
Diphenhydramine
HCL 5 mg/kg/24 hrs (O) in 3 to 4 div doses.
Pheniramine maleate 1.5 mg/kg/24 hrs Oral or IM.
Promethazine HCL 0.5 mg/kg/dose (full dose as antihistaminic at night, quarter dose a.m)
Hypnotic—0.5-1 mg/kg/dose IM (avoid in children under 2 years).
Cetirizine 2.5-5 mg/day for children 2-6 years, 5-10 mg for children 6-12
years (not recommended routinely for children under 2 years).
 Annexure 3: Drugs and Drug Dosage 353

TRANQUILIZERS
Chlordiazepoxide HCI 0.5 mg/kg/24 hrs (O).
Chlorpromazine HCI 2 mg/kg/24 hrs 4 to 6 div doses (O).
Diazepam 0.2 to 0.3 mg/kg/24 hrs (O) in 3 4 div doses.
Imipramine HCI 1.5 mg/kg/24 hrs in 3 div doses (may increase up to 50 mg an
hour before bedtime). 50 to 75 mg single dose—over 12 years
(for nocturnal enuresis).
Promethazine HCL 0.5 mg/kg/dose (O) or IM (avoid in children under 2 years).
Haloperidol 0.01 mg/kg/(max 0.5 mg) daily increase up to 0.01 mg/kg/
dose every 12 hours (rarely up to 2 mg/kg/dose).

ANTICONVULSANTS
Carbamazepine 10 mg/kg/24 hrs to begin with increase up to 20 mg/kg/24 hrs
gradually.
Lonazepam 0.05-0.1 mg/kg IV given slowly over 15 minutes, repeat if needed
after 15 minutes.
Clonazepam 0.05 mg/kg/24 hrs to begin with 0.05 mg/kg/wk increase, up
to a max of 0.2 mg/kg/24 hrs.
Ethosuximide 20 mg/kg/24 hrs increase to maximum of 40 mg/kg/24 hrs.
Nitrazepam 0.2 mg/kg/24 hrs increase slowly to 1.0 mg/kg/24 hrs.
Paraldehyde 0.15 mg/kg/ IM (1 ml per year of age) max 5 ml as stat dose
(rectal paraldehyde is also useful given diluted with mineral
oil).
Phenobarbitone 3-5 mg/kg/24hrs oral, 10-20 mg/kg IV stat as a loading dose.
Phenytoin 5 mg/kg/24 hrs oral, 10-20 mg/kg as loading dose IV stat
given very slowly for persisting or recurrent seizures. 5-10 mg/
kg/day q 8 hrs as maintenance.
Pyridoxine 5 mg twice daily (up to100 mg) (O).
Sodium valporate 10 mg/kg/24 hrs (O) to begin with increase by 5 mg/kg/every
week to reach the max of 30-40 mg/kg/24 hrs.
Vigabatrin 50-100 mg/kg/24 hrs
Gabapentin 60 mg/kg/24 hrs
(Further experience is neded regarding the use of vigabatrin and gabapentin in
pediatric age group)

SEDATIVES AND HYPNOTICS

Triclofos Tricloryl (500 mg/5 ml) 50 mg/kg/24 hrs (O) (sedative) 50-75
mg/kg/dose (hypnotic).
Antihistamines Promethazine (Avoid in children under 1 year) 1 mg/kg/24 hrs
(sedative). (Quartr dose every 6 hours in day hours. Half dose
at bedtime).
Benzadiazepines Diazepam inj (5mg/ml) 0.3-0.5 mg/kg IV.
Lorazepam (2 mg/ml): 0.05 mg/kg IV.
Opiates Morphine sulfate 0.1-0.2 mg/kg/IM.
Pethidine (50 mg/ml) 1-2 mg/kg/IV/IM repeated every 6 hrs (max 6
mg/kg/24 hrs).
Pentazocine Fortwin 30 mg/ml 1 mg/kg/IM or SC per dose 500 mcg/kg IV
per dose
354 Selected Topics in Pediatrics for Practitioners

Barbiturates Thiopental (pentathol) (250 mgvial).

2-3 mg/kg IV: Phenobarbitone 5-8 mg/kg/24 hrs (O).
Ketamine 1-2 mg/kg IV 5-10 mg/kg IM
Codeine phosphate 3 mg/kg/24 hrs in 6 div doses.

ANTIEMETICS
Promethazine 0.25 mg to 0.5 mg/kg/dose—repeat 6 hrs later.
Metoclopramide 0.1-0.5 mg/kg/24 hrs for infants under 1 year.
0.5-1.0 mg/kg/24 hrs for older children in 3 div doses.
Domperidone 0.3-0.6 mg/kg/24 hrs in 3 div doses
Cisapride 0.15-0.3 mg/kg/24 hrs in 3 div doses.

ANTIULCER/REFLUX ESOPHAGITIS
Omeprazole 0.4-0.8 mg/kg/24 hours (O) in 1-2 div doses (max 20 mg/day).

VITAMINS AND MINERAL VITAMINS DAILY REQUIREMENTS

Vitamin A 1500 to 5000 IU
Thiamine 0.5 to 1.5 mg
Riboflavin 0.6 to 2 mg
Niacin 20 mg
Vitamin C 30 to 50 mg
Vitamin B12 1 to 5 microgram
 Annexure 4
Vital Statistics—India
HPS Sachdev, Pyush Gupta

Vital statistics are referred to a systemically collected and compiled data relating to
vital events of life such as birth, death, marriage, divorce, adoption etc. These reflect
the health profile of the community and form a basic tool for evaluating the adequacy
of the health care delivery system. No health department can claim to serve efficiently
and effectively without the help of vital statistics.
In India, the main source of vital statistics include the census, registration records
of vital events such as birth and deaths and sample registration system (SRS). SRS
obtains annual information on birth and death rates, fertility rates and age specific
mortality rates in the country through a combination of continuous registration and
half yearly surveys.

Mortality, Fertility and other Health Indicators

Current status of various indicators related to mortality, fertility, life expectancy,
family welfare program, literacy status, immunization coverage and nutrition status
are summarized in Table 1. Deaths in infancy constitute 18.5 percent of total deaths
in India. More than fifty percent of these occur in neonatal period. Infant mortality
rate (IMR) of the country is not representative of its states. Orissa and MP contribute
maximally to the infant mortality (98 per 1000 live births) with the maximum IMR
being achieved by Kerala (16 per 1000 live births).

National Population Policy

With the birth of ‘Astha’ on 11th May 2000 at Safdurjung Hospital, New Delhi, India
was projected to have 1 billion (100 crore) people, i.e. 16 percent of the world’s
population on 2.4 percent of the globe’s land area. The National Population Policy,
2000 (NPP 2000) provides a policy framework for advancing goals and prioritizing
strategies during the next decade to meet the reproductive and health needs of the
people of India. In pursuance of the objectives laid out in NPP 2000, the following
National Socio-Demographic goals to be achieved in each case by 2010 are formulated.
Interestingly, the population of children below 15 years of age (currently 35 percent)
is projected to decline to 28 percent by 2016.
Table1: Fertility, mortality and other health indicators
Fertility indicators
Crude birth rate 26.4 (1998)
General fertility rate 118.3 (1994)
Total fertility rate 3.3 (1998)
Gross Reproduction rate 1.74 (1998)
Natural growth rate 17.4 (1998)
Annual number of births 26,106 thousands (1995)
356 Selected Topics in Pediatrics for Practitioners

Mortality Indicators
Crude death rate 9.0 (1998)
Infant mortality rate 72.0 (1998)
Neonatal mortality rate 47.7 (1994)
Postneonatal mortality rate 26.0 (1994)
Perinatal mortality rate 42.5 (1994)
Stillbirth rate 8.9 (1994)
Child mortality rate 23.9 (1996)
Maternal mortality ratio 407 (1997)
Annual number of under five deaths 3002 thousand (1995)
Life expectancy at birth
Males 62.36yr
Females 63.39yr (1996-2001)
Literacy rate
Males 64.1%
Females 39.3%
Total 52.2% (1991)
Couple protection rate 44.0% (1999)
Immunization coverage
BCG 97.0% (1998-99)
DPT 92.8% (1998-99)
OPV 94.3% (1998-99)
Measles 87.3% (1998-99)
Nutrition Indicators
Low birth weight newborns 33%
% of children who are breastfed
in neonatal period 95.1 (NFHS 1993)
exclusively (0-3mo) 51 (1990-96)
at 1 year 89.2 (NFHS 1993)
% of underfives suffering from
underweight (moderate+severe) 53 (1990-96)
wasting (moderate + severe) 18
stunting (moderate + severe) 52
Total goitre rate (6-11 yr) 9 (1985-94)
 Annexure 5
National Socio-demographic
Goals for 2010
1. Address the unmet needs for basic reproductive and child health services,
supplies and infrastructure.
2. Make school education up to age 14 free and compulsory, and reduce drop outs
at primary and secondary school levels to below 20 percent for both boys and
girls
3. Reduce infant mortality rate to below 30 per 1000 live births.
4. Reduce maternal mortality ratio to below 100 per 100,000 live births.
5. Achieve universal immunization of children against all vaccine preventable
diseases.
6. Promote delayed marriage for girls, not earlier than age 18 and preferably after
20 year of age.
7. Achieve 80 percent institutional deliveries and 100 percent deliveries by trained
persons.
8. Achieve universal access to information/counseling, and services for fertility
regulation and contraception with a wide basket of choices.
9. Achieve 100 percent registration of births, deaths, marriage and pregnancy.
10. Contain the spread of Acquired Immunodeficiency Syndrome (AIDS), and
promote greater integration between the management of reproductive tract
infections (RTI) and sexually transmitted infections (STI) and the National AIDS
Control Organization.
11. Prevent and control communicable diseases.
12. Integrate Indian Systems of Medicine (ISM) in the provision of reproductive and
child health services, and in reaching out to households.
13. Promote vigorously the small family norm to achieve replacement levels of TFR.
14. Bring about convergence in implementation of related social sector programs so
that family welfare becomes a people centered program.
Text and tables adapted from Vital Statistics-India, National Socio - Demographic goals
for 2010, Piyush Gupta, HPS Sachdev, IAP Text Book of Pediatrics, II edn eds Dr. A.
Parthasarathy, PSN Menon, MKC Nair, Jaypee Bros., Medical Publishers, New Delhi 2003.
 Annexure 6
Children’s Forum Message—
A World Fit for Us
We are the world’s children.
We are the victims of exploitation and abuse.
We are street children.
We are the children of war.
We are the victims and orphans of HIV/AIDS.
We are denied good-quality education and health care.
We are victims of political, economic, cultural, religious and environmental
discrimination.
We are children whose voices are not being heard: it is time we are taken into
account.
We want a world fit for children, because a world fit for us is a world fit for
everyone.
In this world,

We see Respect for the Rights of the Child

 governments and adults having a real and effective commitment to the principle
of children’s rights and applying the Convention on the Rights of the Child to
all children,
 safe, secure and healthy environments for children in families, communities and
nations.

We see an end to Exploitation, Abuse and Violence

 laws that protect children from exploitation and abuse being implemented and
respected by all,
 centers and programs that help to rebuild the lives of victimized children.

We see an end to War

 world leaders resolving conflict through peaceful dialogue instead of by using
force,
 child refugees and child victims of war protected in every way and having the
same opportunities as all other children.
 disarmament, elimination of the arms trade and an end to the use of child
soldiers.

We see the Provision of Health Care

 affordable and accessible life-saving drugs and treatment for all children,
 strong and accountable partnerships established among all to promote better
health for children.
 Annexure 6: Children’s Forum Message—A World Fit for Us 359

We see the Eradication of HIV/AIDS

 educational systems that include HIV prevention programs,
 free testing and counselling centres,
 information about HIV/AIDS freely available to the public,
 orphans of AIDS and children living with HIV/AIDS cared for and enjoying the
same opportunities as all other children.
Message from the Children’s Forum, delivered to the UN General Assembly
Special Session on Children by under-18 delegates on 8 May 2002.
Distributed by UNICEF.

BIBLIOGRAPHY
1. Annual Report. Ministry of Health and Family Welfare. Govt. of India
1997-98.
2. Carol Bellamy. The State of the World’s Children 2003, UNICEF, 2002: 84-119.
3. Health and Population Indicators, Department of Family Welfare. Government
of India, (from http://mohfw.nic.in/mmenu.htm) 1999.
4. National Population Policy, Ministry of Health and Family Welfare, Government
of India 2000.
5. Piyush Gupta, HPS Sachdev. Vital Statistics-India, National sociodemographic
goals. In A.Parthasarathy, PSN Menon, MKC Nair (Eds): IAP Textbook of Pediatrics
(2nd edn) 2003. Jaypee Bros Medical Publishers: New Delhi. 2003;956-57.
6. Ramji S, Sachdev HPS. Fertility and mortality indicators. Indian Pediatr
1996;33;877-81.
7. The State of the World’s Children, UNICEF 1999.
 Index

A Articulation disorders 242

Association of chronic constipation 151
Abandoned child 266 Attention deficit disorders 248
Abdomen and genitalia 7 Auditory steady state evoked response 259
ACTH injection 76 Autism spectrum disorders 248
Acute Auto destruct syringes 51
diarrhea antimicrobes
for specific cause 124
B
diarrheal disease 123
dysentery 124 Babies at risk for hypothermia 15
glomerulonephritis 167 Bacterial
nephritic syndrome 167 infection 66
post-streptococcal glomerulonephritis meningitis 79
167 Bag mask ventilation 193
Adolescence 294 Balanced diets for children 46
Adolescent Behavioral observation audiometry 256
care 276 Benefits of exclusive breastfeeding 42
nutrition 281 Benign viral infections 66
sexuality 284 Beta blockers 92
viodence 299 Bilirubin encephalopathy 23
AFP surveillance 53 Bismuth subsalicylate 130
Algorithm for management of acute Body mass index 30
severe asthma 106 Body
Aluminium phosphide and proportion 30
zinc phosphide 205 surface area 217
Amikacin 344 Bowel
Amineptine 214 cleansing 154
Amitriptyline 214 training 149
Amniotic fluid 338 Breakup energy expenditure 46
Amoxapine 214 Breastfeeding 16
Analgesics and antipyretics 352 child health 44
Anthelmintics 350 mother’s medication 44
Antiamoebic drugs 349 technique 16
Antibiotics 344 Bronchial asthma 94
Anticonvulsants 353 acute severe 100
Antidotes 202 guidelines for diagnosis of 98
Antiemetics 354 management 100
Antigiardiasis drugs 350 persistent 107
Antihistaminics 352 Bronchodilators 351
Antihypertensive drugs 351 Burden of adolescent problems 277
Anti-inflammatory therapy 86 Buserelin 180
Antimalarials 349
Antimicrobial therapy 220
Antiulcer/reflux esophagitis 354 C
Antiviral drugs 351 Camphor poisoning 207
Apgar score 8 Captopril 91, 351
Arthritis 83 Caput succedaneum 7
362 Selected Topics in Pediatrics for Practitioners

Cardiomegaly 83 Designing medical research 231

Cardiopulmonary resuscitation 2 Deslorelin 180
Carditis 83 Developmental
Care of normal newborn in labour room 5 assessment general rules of 37
Cationic detergents 207 history 36
Causes language disorders 247
growth delay 33 screening 36
selective delay in motor milestones 41 chart 37
selective language delay 41 Dialysis 202
Central Dietary modification 155
adoption resource agency 268 Digoxin 350
precocious puberty 179 Disimpaction 154
Cephalhematoma 7 Dothiepin 214
Cephalosporins 346 Drugs and drug dosage 344
Chemotherapeutics 348
Child adoption in India 263 E
Child survival and safe motherhood 2
Childhood aphasia 248 Early detection of serious problem 18
Children with EEGs
mild hearing loss 254 ambulatory 77
profound hearing losses 254 video 77
Circumference Enalapril 91
chest 31 Encopresis 147
head 31 Enemas 154
Clomipramine 214 Enteric fever 69
Clonazepam 76 Epidemiology 82
Coagulation abnormalities 171 Epilepsy
Cohort 234 management 74
Combination vaccines 60 types of 77
Common problems in the newborn 18 Erythema
Communication disorder 237 marginatum 84
Conducting sex and sexuality sessions 286 toxicum 19
Congenital Esophageal atresia 227
hypothyroidism 173 Essential newborn care 4
teeth (natal teeth) 19 Etiopathogenesis 82
Congestive cardiac failure Evaluation 33
diagnosis of 89 Evoked response audiometry 258
hemodynamic classification 88 Evolving healthy sexuality 284
treatment 89 Examination of newborn
protocol of 93 after normal delivery 6
Constipation and encopresis 147 Exomphalos 229
Constitutional growth delay and
puberty 33 F
Consumer Protection Act 2 Factors
Criteria for weaning 105 antepartum 8
Critically ill child 189 intrapartum 8
Cyanosis 199 related to family 280
Familial short stature 33
D Family life education for adolescents 281
Daily calorie requirements 46 Fecal
Daily requirement for water 46 incontinence 148
Depression in children 293 soiling 148
 Index 363

Fever Imperforate anus and rectum 229

in a high-risk child 71 Infant and young child feeding 42
management of 71 Influenza vaccine 59
without focus 68 Inhaled steroids 107
Fluency disorders 244 Inotropes 90
Fluid therapy 340 Institutional child syndrome 274
Fluoroquinolones 348 Integrated management of neonatal 2
Foreign sponsoring agency 270 Inter country adoptions 264
Interchangeability of vaccine
G formulations 51
Intracellular fluid 341
Gastric lavage 201 Intraosseous access 194
Gastrointestinal diseases 44 Iron ingestion 210
Gentamicin sulfate 344 Irrational combinations 218
Gentle stimulation to breathe 10
Gestational
age groups 4 J
assessment 7 Jacobson’s progressive 309
Glomerular sclerosis 171 Jaundice
Group breast milk 24
elective 228, 230 causes of 23
emergency 227 in newborn 22
intermediate 228 pathological 23
semi emergency 229 phototherapy 24
Growth
chart 31
hormone therapy 187 K
monitoring 29
Guardian and Wards Act 268 Kangaroo mother care 15
Kerosene ingestion 203
H
L
Hashimoto’s thyroiditis 176
Hearing losses 252 Lamotrigine 76
Heart rate 191 Language intervention 251
Hemophilus influenzae 57 Lavage 154
Hirschsprung’s disease 152, 155 Leptospirosis 69
Histerelin 180 Leuprolide acetate 179
Home care for preterm and SGA babies 22 Levetiracetam 76
Hormone levels in serum and urine 334 Life skill development 282

I
M
Ideal thermometer 63
Immunization Macrolides and related drugs 347
adolescent 54 Magnesium sulphate 103
adult 49 Magnitude of the problem 238
coverage 53 Maintenance therapy 341
general rules of 55 Malaria 66, 69
in practice 49 Management of
infant 49 lowbirth weight 19
program 53 specific poisons 196
schedules 49 Management protocol 177
time table 54 Maternal and child health 2
toddler 49 Meconium aspiration syndrome 13
364 Selected Topics in Pediatrics for Practitioners

Medroxyprogesterone acetate 178 Order of priority 265

Metals and binding proteins 331 Otoacoustic emissions 258
Metaprolol 92
Methods of heat loss in newborn 14 P
Milestones in speech 241
Milia 19 Peak expiratory flow rate 98
Milrinone 91 Pediatric surgical referrals 226
Minor manifestations 84 Pediatrician in the year 2033 321
Miosis 199 Pediatricians and adoption 273
Modified penicillins 345 Penicillin 345
Mongolian spots 19 Personal hygiene 281
Morpheme 240 Pervasive developmental disorders 248
Motor activity 190 Phenobarbital 76
Muscarine 209 Phenytoin 76
Muscle tone 191 Pneumococcal polysaccharide vaccine 59
Mydriasis 199 Poisoning
in children 196
statistics 197
N
type of toxins 197
Nafarelin 179 Polyarthritis 86
Naphthalene 207 Post ICU plan 105
National immunization days 53 Post polio eradication policy 52
National population policy 355 Post resuscitation care 12
Neem oil ingestion 205 Practical points for breastfeeding 44
Neonatal Predictivity of the test 325
cholestasis 132 Prefixes 327
emergencies 227 Premarital counseling 287
hepatitis 132 Preparation for resuscitation 9
sepsis 26 Preterm babies have the following risks
early onset 26 20
Nephrotic syndrome 169 Principles in resuscitation 9
minimal changes 170 Problematic viral infections 66
Netilmicin sulfate 344 Prolonged fever 69
Neurological examination 36 Psychosocial aspects of asthma
Newborn management 111
care at delivery 14 Pulmonary score index 101
period 22 Pupil size 191
unit 14 Purgation 155
Newer anticonvulsants 76 Pyrexia of unknown origin 70
Nicotine 209
Nitroglycerin 92
Nonstreroidal anti-inflammatory drug 352 Q
Normal
Qualities of a good life partner 288
bowel habits 148
Quiet tachypnoea 191
hematological values 327
laboratory values 325
urinary values 336 R

O Randomized controlled clinical trial 234

Rat killer poison 205
Occult bacteremia 66 Rational drug therapy 216, 220
Oral Recent trends in the diagnosis 79
live attenuated polio vaccine 52 Recognition of preterm and SGA babies 20
rehydration therapy 2 Recording 31
 Index 365

Recurrent fever 71 Sweat 339

Referral for diagnosis 226 Sydenham’s chorea 84
Requirements for normal delivery 5
Research question 233 T
Respiratory
distress in newborn 25 Teenage morbidity in the community
rate 191 278
syncytial virus 95 Tetracyclines 347
Resuscitation Therapy
equipments needed 9 specific 27
in presence of meconium 13 supportive 27
Retracted nipple 17 Thumb method 11
Review of the literature 233 Thyroid function tests 174
Rheumatic fever 82 Tigabine 76
primary prevention of 87 Tobramycin 344
secondary prevention 87 Toxidromes 200
Rhinitis 112 Tranquilizers 353
Role of pediatrician 298 Transport
Routine care of newborn 14 preparation for 28
Scan provision of other care 28
DMSA 164 provision of warm 28
DTPA 164 of neonatal 27
Scholastic backwardness 279 Traumatic brain injury 248
Sedatives and hypnotics 353 Tricyclic antidepressant 214
Semantics 240 Trigger factors 96
Separation anxiety 274 Trivandrum developmental scale 37
Serum Tryptorelin 180
biochemistry 330 Tuberculosis 69
enzyme levels 332 bactec system 116
vitamin levels 339 childhood 114
Sexuality culture of the tubercle bacilli 116
problems in adolescence 284 disseminated 115
the sum total 287 investigation 115
transmitted infections 304 management 117
SGA baby 20 Mantoux test 116
Short and fat child 33 morphology of mycobacterium 114
Short-term fever 65 natural course of primary infection
Simple acute constipation 153 115
Sinusitis 112 primary complex 115
Skin care 18 progressive primary complex 115
Sodium nitroprusside 91 reinfection 114
Special needs 274
Spirometry 99 U
Steroids 102 Umbilical
Stool specimen 338 cord care 18
Streptomycin sulfate 344 granuloma 19
Study report Universal immunization 2
child 267 Urinary tract infection 69, 160-163
home 266 clinical features 161
Subconjunctival hemorrhages 19 diagnosis 161
Subcutaneous nodules 84 history and clinical examination 162
Suppository 155 importance of 160
Surrendered child 265 initial evaluation 162
366 Selected Topics in Pediatrics for Practitioners

neonates and young infant 161 Voice disorders 246

older children 161 Voiding cystourethrogram 164
subsequent evaluation 163 Vomiting 18

V W
Vaginal bleeding and discharge 19 Warfarin 206
Valvulitis 83 Warm chain 15
Vancomycin 348 Warmth 14
Vasoactive intestinal peptide 95 Water loss 341
Vernacular magazine 287 Whole bowel irrigation 201
Vigabatrine 76 Work of breathing 191
Viral infections 95, 112
Visual reinforcement audiometry 257
Z
Vital signs 7
Vital statistics 355 Zinc supplementation 128
Vitamin A supplementation 129 Zonisamide 76